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Bio 139 > Chapter 19 Blood > Flashcards

Chapter 19 Blood Flashcards

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1
Q

Blood contributes to homeostasis by

A

transporting oxygen, carbon dioxide, nutrients, and hormones to and from your body’s cells. It also helps regulate body pH and temperature, and provides protection against disease through phagocytosis and the production of antibodies.

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2
Q

The cardiovascular system (cardio- = heart; vascular = blood vessels) consists of three interrelated components which are

A

blood, the heart, and blood vessels

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3
Q

hematology is

A

The branch of science concerned with the study of blood, blood-forming tissues, and the disorders associated with them

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4
Q

Blood is

A

a liquid connective tissue that consists of cells surrounded by a liquid extracellular matrix.

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5
Q

Interstitial fluid is

A

the fluid that bathes body cells (see Figure 27.1) and is constantly renewed by the blood.

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6
Q

What are the three funcrions of blood

A

Transportation
Regulation
and Protection

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7
Q

Describe how blood functions in transportation

A

blood transports inhaled oxygen from the lungs to the cells of the body and carbon dioxide from the body cells to the lungs for exhalation. It carries nutrients from the digestive canal to body cells and hormones from endocrine glands to other body cells. Blood also transports heat and waste products to various organs for elimination from the body.

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8
Q

Describe how blood functions in regulation

A

Circulating blood helps maintain homeostasis of all body fluids. Blood helps regulate pH through the use of buffers (chemicals that convert strong acids or bases into weak ones). It also helps adjust body temperature through the heat-absorbing and coolant properties of the water (see Section 2.4) in blood plasma and its variable rate of flow through the skin, where excess heat can be lost from the blood to the environment. In addition, blood osmotic pressure influences the water content of cells, mainly through interactions of dissolved ions and proteins.

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9
Q

Describe how blood functions in protection

A

Blood can clot (become gel-like), which protects against its excessive loss from the cardiovascular system after an injury. In addition, its white blood cells protect against disease by carrying on phagocytosis. Several types of blood proteins, including antibodies, interferons, and complement, help protect against disease in a variety of ways.

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10
Q

Describe the texture of blood

A

Blood is denser and more viscous (thicker) than water and feels slightly sticky.

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11
Q

what is the normal temperature of blood

A

38 Celsius

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12
Q

What is the pH range for normal blood

A

7.35-7.45

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13
Q

The color of blood varies based on

A

oxygen content

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14
Q

Bright red blood is

A

saturated with Oxygen

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15
Q

Dark red blood is

A

unsaturated with oxygen

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16
Q

Blood constitutes about _________ of extracellular fluid, amounting to ______________ of the total body mass.

A

20%

8%

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17
Q

In a male the average blood volume is

A

5-6 liters

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18
Q

In a female the average blood volume is

A

4-5 liters

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19
Q

Several hormones, regulated by negative feedback, ensure that

A

blood volume and osmotic pressure remain relatively constant.

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20
Q

which hormones regulate how much water is excreted in the urine

A

aldosterone, antidiuretic hormone, and atrial natriuretic peptide,

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21
Q

Complete blood count (CBC) is

A

one of the most common blood tests and is often done as part of a regular checkup. It measures the number and size of red blood cells, hemoglobin, and hematocrit; the number and percentage of each type of white blood cell in a sample of 100 cells (differential white blood cell count); and the number of platelets.

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22
Q

Basic metabolic panel refers to

A

a group of tests that measure the levels of different chemicals in blood. Included are glucose, calcium, various electrolytes, blood urea nitrogen, and creatinine.

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23
Q

Blood enzyme tests. are used to

A

determine the levels and activity of certain enzymes as indicators of organ damage. For example, higher levels of creatine kinase and troponin indicate damage to the heart and skeletal muscles, while higher levels of ALT and AST indicate liver damage.

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24
Q

Lipoprotein panels are

A

several tests that assess the risk of heart disease. Among the blood components measured are total cholesterol, HDL, LDL, and triglycerides.

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25
Q

What are the two components of blood

A

blood plasma
formed elements

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26
Q

What is blood plasma,

A

a watery liquid extracellular matrix that contains dissolved substances,

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27
Q

What are formed elements,

A

cells and cell fragments.

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28
Q

Blood is about 55% ___________ and 45% ___________________

A

blood plasma
formed elements

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29
Q

99 percent of formed elements are

A

RBC’s

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30
Q

Pale, colorless white blood cells (WBCs) and platelets occupy

A

less than 1% of the formed elements.

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31
Q

buffy coat

A

layer of WBC’s between the packed RBCs and blood plasma in centrifuged blood

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32
Q

When the formed elements are removed from blood

A

, a straw-colored liquid called blood plasma (or simply plasma) is left.

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33
Q

Blood plasma is about _______________ water and ____________ solutes

A

91.5%

8.5%

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34
Q

What are blood plasma protiens

A

proteins that are confined to blood

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35
Q

Blood palsma proteins include

A

the albumins (al′-BŪ-mins) (54% of blood plasma proteins), globulins (GLOB-ū-lins) (38%), and fibrinogen (fī-BRIN-ō-jen) (7%).

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36
Q

Certain blood cells develop into plasmocytes that produce gamma globulins, an important type of globulin

A

These blood plasma proteins are also called antibodies or immunoglobulins (im′-ū-nō-GLOB-ū-lins) because they are produced during certain immune responses.

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37
Q

What is an antigen

A

Foreign substances such as bacteria and viruses stimulate production of millions of different antibodies

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38
Q

The formed elements of the blood include three principal components:

A

red blood cells, white blood cells, and platelets (Figure 19.2).

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39
Q

RBC’s function is to

A

transport oxygen from the lungs to body cells and deliver carbon dioxide from body cells to the lungs.

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40
Q

White blood cells (WBCs) or leukocytes function is to

A

protect the body from invading pathogens and other foreign substances.

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41
Q

Platelets

A

Fractions of cells that release chemicals that promote blood clotting when blood vessels are damaged. Platelets are the functional equivalent of thrombocytes, nucleated cells found in lower vertebrates that prevent blood loss by clotting blood.

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42
Q

Platelets are the functional equivalent of

A

thrombocytes, nucleated cells found in lower vertebrates that prevent blood loss by clotting blood.

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43
Q

hematocrit

A

The percentage of total blood volume occupied by RBCs

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44
Q

The normal range of hematocrit

A

for adult females is 38–46% (average = 42); for adult males, it is 40–54% (average = 47)

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45
Q

The hormone testosterone, present in much higher concentration in males than in females, stimulates synthesis of

A

erythropoietin (EPO), the hormone that in turn stimulates production of RBCs

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46
Q

A significant drop in hematocrit indicates

A

anemia, a lower-than-normal number of RBCs

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47
Q

In polycythemia (pol′-ē-sī-THĒ-mē-a)

A

the percentage of RBCs is abnormally high, and the hematocrit may be 65% or higher. This raises the viscosity of blood, which increases the resistance to flow and makes the blood more difficult for the heart to pump. Increased viscosity also contributes to high blood pressure and increased risk of stroke.

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48
Q

Causes of polycythemia include

A

abnormal increases in RBC production, tissue hypoxia, dehydration, blood doping, or the use of erythropoietin by athletes.

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49
Q

The liquid portion of blood is

A

water

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50
Q

What is the function of water in blood

A

Solvent and suspending medium. Absorbs, transports, and releases heat.

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51
Q

Where are blood plasma protiens generally produced

A

Liver

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52
Q

What is the function of blood plasma protiens

A

Responsible for colloid osmotic pressure. Major contributors to blood viscosity. Transport hormones (steroid), fatty acids, and calcium. Help regulate blood pH

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53
Q

Describe albumins

A

Smallest and most numerous plasma proteins.

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54
Q

What is the function albumins

A

Help maintain osmotic pressure, an important factor in the exchange of fluids across blood capillary walls.

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55
Q

Describe globulins

A

Large proteins (plasmocytes produce immunoglobulins).

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56
Q

What is the function of globulins

A

Immunoglobulins help attack viruses and bacteria. Alpha and beta globulins transport iron, lipids, and fat-soluble vitamins.

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57
Q

Fibrinogen is

A

a large blood plasma protien that plays an essential role in clotting

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58
Q

What are some of the electrolytes found in blood plasma

A

Inorganic salts; positively charged (cations) Na+, K+, Ca2+, Mg2+; negatively charged (anions) Cl−, HPO42−, SO42−, HCO3−.

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59
Q

What is the function of electrolytes in plasma

A

Help maintain osmotic pressure and play essential roles in cell functions.

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60
Q

Describe the nutrients found in blood plasma

A

Products of digestion, such as amino acids, glucose, fatty acids, glycerol, vitamins, and minerals.

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61
Q

What is the function of blood plasma

A

Essential roles in cell functions, growth, and development.

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62
Q

What gases are found in blood plasma

A

Oxygen
Carbon dioxide
Nitrogen

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63
Q

Oxygen in blood plasma

A

is important to many cellular functions

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64
Q

What is the function of Carbon Dioxide in blood

A

Involved in the regulation of blood pH.

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65
Q

Nitrogen in blood plasma

A

has no known function

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66
Q

What regulatory substances are in blood plasma

A

Enzymes
Hormones
Vitamins

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67
Q

What is the function of enzymes in plasma

A

They catalze chemical reactions

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68
Q

What is the functions of hormones in plasma

A

Regulate metabolism, growth, and development.

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69
Q

What is the function of vitamins in blood plasma

A

Cofactors for enzymatic reactions.

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70
Q

What waste products exist in blood plasma

A

Urea, uric acid, creatine, creatinine, bilirubin, ammonia.

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71
Q

Why do waste products appear in plasma

A

Most are breakdown products of protein metabolism that are carried by the blood to organs of excretion.

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72
Q

Negative feedback systems regulate

A

the total number of RBCs and platelets in circulation, and their numbers normally remain steady

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73
Q

The abundance of the different types of WBCs

A

varies in response to challenges by invading pathogens and other foreign antigens

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74
Q

hemopoiesis (hēm-ō-poy-Ē-sis; -poiesis = making) or hematopoiesis.

A

The process by which the formed elements of blood develop

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75
Q

Red bone marrow becomes

A

the primary site of hemopoiesis in the last 3 months before birth, and continues as the source of blood cells after birth and throughout life.

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76
Q

Red bone marrow

A

is a highly vascularized connective tissue located in the microscopic spaces between trabeculae of spongy bone tissue.

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77
Q

About 0.05–0.1% of red bone marrow cells are called

A

multipotent (mul-TIP-ō-tent; multi = many) stem cells or hemocytoblasts and are derived from mesenchyme (tissue from which almost all connective tissues develop). These cells have the capacity to develop into many different types of related cells

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78
Q

Under certain conditions, such as severe bleeding,

A

yellow bone marrow can revert to red bone marrow; this occurs as blood-forming stem cells from red bone marrow move into yellow bone marrow, which is then repopulated by multipotent stem cells.

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79
Q

As an individual ages,

A

the rate of blood cell formation decreases; red bone marrow in the medullary cavity of long bones becomes inactive and is replaced by yellow bone marrow, which consists largely of fat cells.

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80
Q

Multipotent stem cells in red bone marrow

A

reproduce themselves, proliferate, and differentiate into cells that give rise to blood cells, macrophages, reticular cells, mast cells, and adipocytes

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81
Q

After blood cells form,

A

they enter the sinuses and other blood vessels and leave the bone through nutrient and periosteal veins

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82
Q

With the exception of lymphocytes, formed elements do not

A

divide once they leave red bone marrow.

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83
Q

In order to form blood cells, multipotent stem cells in red bone marrow

A

produce two further types of stem cells, which have the capacity to develop into several types of cells. These stem cells are called myeloid stem cells and lymphoid stem cells

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84
Q

Myeloid stem cells begin their development

A

in red bone marrow

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85
Q

Myeloid stem cels give rise to

A

red blood cells, platelets, monocytes, neutrophils, eosinophils, basophils, and mast cells.

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86
Q

Lymphoid stem cells give rise to

A

Lymphocytes and natural killer cells

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87
Q

During hemopoiesis, some of the myeloid stem cells differentiate into

A

progenitor cells

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88
Q

Progenitor cells are no longer capable of

A

reproducing themselves and are committed to giving rise to more specific elements of blood.

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89
Q

Some progenitor cells are known as

A

colony-forming units

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90
Q

CFU–E ultimately produces

A

erythrocytes (red blood cells)

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91
Q

CFU–Meg produces

A

megakaryocytes the source of platelets

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92
Q

CFU–GM ultimately produces

A

granulocytes (specifically, neutrophils) and monocytes

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93
Q

Progenitor cells and stem cells

A

resemble lymphocytes and cannot be distinguished by their microscopic appearance alone.

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94
Q

bone marrow aspiration

A

withdrawal of a small amount of red bone marrow with a fine needle and syringe

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95
Q

bone marrow biopsy

A

removal of a core or cylindrical sample of red bone marrow with a larger needle

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96
Q

progenitor cells give rise to

A

precursor cells, also known as blasts

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97
Q

Precursor cells have

A

recognizable microscopic appearances.

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98
Q

Several hormones called hemopoietic growth factors (hē-mō-poy-ET-ik) regulate

A

the differentiation and proliferation of particular progenitor cells.

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99
Q

Erythropoietin (EPO) (e-rith′-rō-POY-ē-tin) functions to

A

Erythropoietin (EPO) (e-rith′-rō-POY-ē-tin) increases the number of red blood cell precursors

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100
Q

Erythropoietin abbreviation

A

EPO

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101
Q

EPO is produced primarily by cells in the

A

kidneys that lie between the kidney tubules

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102
Q

With renal failure,

A

EPO release slows and RBC production is inadequate. This leads to a decreased hematocrit, which leads to a decreased ability to deliver oxygen to body tissues.

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103
Q

Thrombopoietin (TPO) (throm′-bō-POY-ē-tin)

A

is a hormone produced by the liver that stimulates the formation of platelets from megakaryocytes.

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104
Q

Thrombopoietin abbreviation

A

(TPO)

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105
Q

Cytokines (SĪ-tō-kīns) are

A

small glycoproteins that are typically produced by cells such as red bone marrow cells, leukocytes, macrophages, fibroblasts, and endothelial cells.

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106
Q

Cytokines function is to

A

stimulate proliferation of progenitor cells in red bone marrow and regulate the activities of cells involved in nonspecific defenses (such as phagocytes) and immune responses

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107
Q

Two important families of cytokines that stimulate white blood cell formation are

A

colony-stimulating factors (CSFs) and interleukins

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108
Q

Cytokines generally act as

A

local hormones

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109
Q

Red blood cells (RBCs) or erythrocytes (e-RITH-rō-sīts; erythro- = red; -cyte = cell) contain

A

the oxygen-carrying protein hemoglobin, which is a pigment that gives whole blood its red color

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110
Q

To maintain normal numbers of RBCs,

A

new mature cells must enter the circulation at the astonishing rate of at least 2 million per second, a pace that balances the equally high rate of RBC destruction.

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111
Q

Describe the shape of RBC’s

A

RBCs are biconcave discs with a diameter of 7–8 μm

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112
Q

RBC’s plasma membranes are

A

both strong and flexible, which allows them to deform without rupturing as they squeeze through narrow blood capillaries.

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113
Q

RBCs lack

A

a nucleus and other organelles and can neither reproduce nor carry on extensive metabolic activities.

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114
Q

The cytosol of RBCs contains

A

hemoglobin molecules; these important molecules are synthesized before loss of the nucleus during RBC production and constitute about 33% of the cell’s weight.

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115
Q

Red blood cells are highly specialized for

A

their oxygen transport function.

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116
Q

Because mature RBCs have no nucleus,

A

all of their internal space is available for oxygen transport

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117
Q

Because RBCs lack mitochondria and generate ATP anaerobically (without oxygen),

A

they do not use up any of the oxygen they transport.

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118
Q

Why are RBC´s biconcave discs

A

A biconcave disc has a much greater surface area for the diffusion of gas molecules into and out of the RBC than would, say, a sphere or a cube.

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119
Q

A hemoglobin molecule consists of a protein called

A

globin

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120
Q

globin is

A

composed of four polypeptide chains (two alpha and two beta chains); a ringlike nonprotein pigment called a heme (Figure 19.4b) is bound to each of the four chains.

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121
Q

How is hemoglobin able to attach to four oxygen molecules

A

At the center of each heme ring is an iron ion (Fe2+) that can combine reversibly with one oxygen molecule (Figure 19.4c), allowing each hemoglobin molecule to bind four oxygen molecules.

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122
Q

Each oxygen molecule picked up from the lungs

A

is bound to an iron ion.

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123
Q

As blood flows through tissue capillaries,

A

the iron–oxygen reaction reverses. Hemoglobin releases oxygen, which diffuses first into the interstitial fluid and then into cells.

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124
Q

Hemoglobin also transports

A

about 23% of the total carbon dioxide, a waste product of metabolism.

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125
Q

Blood flowing through tissue capillaries picks up

A

carbon dioxide, some of which combines with amino acids in the globin part of hemoglobin.

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126
Q

As blood flows through the lungs, the carbon dioxide is

A

released from hemoglobin and then exhaled.

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127
Q

In addition to its key role in transporting oxygen and carbon dioxide, hemoglobin also plays a role in

A

the regulation of blood flow and blood pressure

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128
Q

The gaseous hormone nitric oxide (NO), produced by the endothelial cells that line blood vessels,

A

binds to hemoglobin.

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129
Q

Under some circumstances, hemoglobin releases NO. The released NO causes

A

vasodilation, an increase in blood vessel diameter that occurs when the smooth muscle in the vessel wall relaxes.

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130
Q

Vasodilation

A

improves blood flow and enhances oxygen delivery to cells near the site of NO release

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131
Q

Red blood cells also contain the enzyme carbonic anhydrase (CA), which

A

catalyzes the conversion of carbon dioxide and water to carbonic acid, which in turn dissociates into H+ and HCO3−

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132
Q

carbonic anhydrase (CA) catalyzes the conversion of carbon dioxide and water to carbonic acid, which in turn dissociates into H+ and HCO3−. The entire reaction is reversible.This reaction is significant for two reasons:

A

(1) It allows about 70% of CO2 to be transported in blood plasma from tissue cells to the lungs in the form of HCO3− (see Chapter 23). (2) It also serves as an important buffer in extracellular fluid (see Chapter 27).

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133
Q

Red blood cells live

A

only about 120 days because of the wear and tear their plasma membranes undergo as they squeeze through blood capillaries.

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134
Q

Without a nucleus and other organelles,

A

RBCs cannot synthesize new components to replace damaged ones

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135
Q

The plasma membrane of RBC´s

A

becomes more fragile with age, and the cells are more likely to burst, especially as they squeeze through narrow channels in the spleen

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136
Q

Ruptured red blood cells are

A

removed from circulation and destroyed by resting phagocytic macrophages in the spleen and liver

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137
Q

What is the first step in the recycling of dead RBC´S

A

Macrophages in the spleen, liver, or red bone marrow phagocytize ruptured and worn-out red blood cells

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138
Q

In the RBC recylcling process, after Macrophages in the spleen, liver, or red bone marrow phagocytize ruptured and worn-out red blood cells

A

The globin and heme portions of hemoglobin are split apart

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139
Q

In the RBC recylcling process, after The globin and heme portions of hemoglobin are split apart what happens to globin

A

Globin is broken down into amino acids, which can be reused to synthesize other proteins.

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140
Q

In the RBC recylcling process, after The globin and heme portions of hemoglobin are split apart. what happens to the heme portion

A

Iron is removed from the heme portion in the form of Fe3+, which associates with the plasma protein transferrin (trans-FER-in; trans- = across; -ferr- = iron), a transporter for Fe3+ in the bloodstream.

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141
Q

In the RBC recylcling process, after Iron is removed from the heme portion in the form of Fe3+, which associates with the plasma protein transferrin

A

In the RBC recylcling process, after In muscle fibers, liver cells, and macrophages of the spleen and liver, Fe3+ detaches from transferrin and attaches to an iron-storage protein called ferritin (FER-i-tin).

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142
Q

In the RBC recylcling process, after Fe3+ detaches from transferrin and attaches to an iron-storage protein called ferritin (FER-i-tin).

A

On release from a storage site or absorption from the digestive canal, Fe3+ reattaches to transferrin.

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143
Q

In the RBC recylcling process after Fe3+ reattaches to transferrin.

A

The Fe3+–transferrin complex is then carried to red bone marrow, where RBC precursor cells take it up through receptor-mediated endocytosis (see Figure 3.12) for use in hemoglobin synthesis. Iron is needed for the heme portion of the hemoglobin molecule, and amino acids are needed for the globin portion. Vitamin B12 is also needed for the synthesis of hemoglobin.

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144
Q

In the RBC recycling process after The Fe3+–transferrin complex is carried to red bone marrow, where RBC precursor cells take it up through receptor-mediated endocytosis (see Figure 3.12) for use in hemoglobin synthesis.

A

Erythropoiesis in red bone marrow results in the production of red blood cells, which enter the circulation.

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145
Q

In the RBC recycling process What happens to the non-iron portion of heme

A

the non-iron portion of heme is converted to biliverdin (bil-ē-VER-din), a green pigment, and then into bilirubin (bil-ē-ROO-bin), a yellow-orange pigment.

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146
Q

In the RBC recycling process after the non-iron portion of heme is eventually converted to bilirubin (bil-ē-ROO-bin)

A

Bilirubin enters the blood and is transported to the liver.

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147
Q

In the RBC recycling process after Bilirubin enters the blood and is transported to the liver.

A

Within the liver, bilirubin is released by liver cells into bile, which passes into the small intestine and then into the large intestine.

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148
Q

In the RBC recycling process after bile passes into the small intestine and then into the large intestine.

A

In the large intestine, bacteria convert bilirubin into urobilinogen (ūr-ō-bī-LIN-ō-jen)

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149
Q

In the RBC recycling process after bacteria convert bilirubin into urobilinogen (ūr-ō-bī-LIN-ō-jen)

A

Some urobilinogen is absorbed back into the blood, converted to a yellow pigment called urobilin (ūr-ō-BĪ-lin), and excreted in urine. Most urobilinogen is eliminated in feces in the form of a brown pigment called stercobilin (ster′-kō-BĪ-lin), which gives feces its characteristic color.

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150
Q

The rate of RBC formation by red bone marrow equals

A

the rate of RBC destruction by macrophages.

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151
Q

Because free iron ions (Fe2+ and Fe3+) bind to and damage molecules in cells or in the blood

A

transferrin and ferritin act as protective “protein escorts” during transport and storage of iron ions

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152
Q

Erythropoiesis (e-rith′-rō-poy-Ē-sis), the production of RBCs, starts in

A

the red bone marrow with a precursor cell called a proerythroblast (prō-e-RITH-rō-blast)

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153
Q

a proerythroblast divides several times, producing cells that

A

begin to synthesize hemoglobin

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154
Q

Ultimately, a cell near the end of the development sequence

A

ejects its nucleus and becomes a reticulocyte

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155
Q

Loss of the nucleus in RBC’s causes

A

the center of the cell to indent, producing the red blood cell’s distinctive biconcave shape.

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156
Q

Reticulocytes pass from red bone marrow into the bloodstream by

A

squeezing between plasma membranes of adjacent endothelial cells of blood capillaries.

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157
Q

Reticulocytes develop into

A

mature red blood cells within 1 to 2 days after their release from red bone marrow.

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158
Q

The rate of erythropoiesis is measured by a

A

reticulocyte count.

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159
Q

Normally, erythropoiesis and red blood cell destruction

A

proceed at roughly the same pace

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160
Q

If the oxygen-carrying capacity of the blood falls because erythropoiesis is not keeping up with RBC destruction,

A

a negative feedback system steps up RBC production

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161
Q

hypoxia

A

An oxygen deficiency at the tissue level

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162
Q

hypoxia may occur if

A

too little oxygen enters the blood.

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163
Q

hypoxia stimulates

A

the kidneys to step up the release of erythropoietin, which speeds the development of proerythroblasts into reticulocytes in the red bone marrow.

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164
Q

As the number of circulating RBCs increases

A

more oxygen can be delivered to body tissues.

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165
Q

Premature newborns often exhibit

A

anemia, due in part to inadequate production of erythropoietin.

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166
Q

During the first weeks after birth,

A

the liver, not the kidneys, produces most EPO.

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167
Q

Because fetal hemoglobin (hemoglobin present at birth) carries up to 30% more oxygen,

A

the loss of fetal hemoglobin, due to insufficient erythropoietin production, makes the anemia worse.

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168
Q

Unlike red blood cells, white blood cells (WBCs) or leukocytes (LOO-kō-sīts; leuko- = white)

A

have nuclei and a full complement of other organelles but they do not contain hemoglobin.

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169
Q

Granular leukocytes include

A

neutrophils, eosinophils, and basophils;

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170
Q

agranular leukocytes include

A

lymphocytes and monocytes

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171
Q

After staining, each of the three types of granular leukocytes displays

A

conspicuous granules with distinctive coloration that can be recognized under a light microscope

172
Q

Describe the appearance of a neutrophil under a micoscope

A

The granules of a neutrophil (NOO-trō-fil) are smaller than those of other granular leukocytes, evenly distributed, and pale lilac (Figure 19.7a). Because the granules do not strongly attract either the acidic (red) or basic (blue) stain, these WBCs are neutrophilic (= neutral loving). The nucleus has two to five lobes, connected by very thin strands of nuclear material. As the cells age, the number of nuclear lobes increases. Because older neutrophils thus have several differently shaped nuclear lobes, they are often called polymorphonuclear leukocytes (PMNs), polymorphs, or “polys.”

173
Q

Describe the appearance of an eosinophil under a light microscope

A

The large, uniform-sized granules within an eosinophil (ē-ō-SIN-ō-fil) are eosinophilic (= eosin-loving)—they stain red-orange with acidic dyes (Figure 19.7b). The granules usually do not cover or obscure the nucleus, which most often has two lobes connected by either a thin strand or a thick strand of nuclear material.

174
Q

Describe the appearance of an basophil under a light microscope

A

The round, variable-sized granules of a basophil (BĀ-sō-fil) are basophilic (= basic loving)—they stain blue-purple with basic dyes (Figure 19.7c). The granules commonly obscure the nucleus, which has two lobes.

175
Q

Even though so-called agranular leukocytes possess cytoplasmic granules

A

, the granules are not visible under a light microscope because of their small size and poor staining qualities.

176
Q

Describe the appearance of a lymphocyte

A

The nucleus of a lymphocyte (LIM-fō-sīt) stains dark and is round or slightly indented (Figure 19.7d). The cytoplasm stains sky blue and forms a rim around the nucleus. The larger the cell, the more cytoplasm is visible. Lymphocytes are classified by cell diameter as large lymphocytes (10–14 μm) or small lymphocytes (6–9 μm). Although the functional significance of the size difference between small and large lymphocytes is unclear, the distinction is still clinically useful because an increase in the number of large lymphocytes has diagnostic significance in acute viral infections and in some immunodeficiency diseases.

177
Q

Describ the appearance of monocytes under a microscope

A

The nucleus of a monocyte (MON-ō-sīt′) is usually kidney-shaped or horseshoe-shaped, and the cytoplasm is blue-gray and has a foamy appearance (Figure 19.7e). The cytoplasm’s color and appearance are due to very fine azurophilic granules (az′-ū-rō-FIL-ik; azur- = blue; -philic = loving), which are lysosomes. Blood is merely a conduit for monocytes, which migrate from the blood into the tissues, where they enlarge and differentiate into macrophages (MAK-rō-fā-jez = large eaters). Some become resting (tissue) macrophages, which means they reside in a particular tissue; examples are alveolar macrophages in the lungs or macrophages in the spleen. Others become wandering macrophages, which roam the tissues and gather at sites of infection or inflammation.

178
Q

White blood cells and all other nucleated cells in the body have

A

proteins, called major histocompatibility (MHC) antigens, protruding from their plasma membrane into the extracellular fluid.These “cell identity markers” are unique for each person (except identical twins)

179
Q

Although RBCs possess blood group antigens,

A

they lack the MHC antigens.

180
Q

In a healthy body, some WBCs, especially lymphocytes, can live

A

for several months or years, but most live only a few days. During a period of infection, phagocytic WBCs may live only a few hours

181
Q

Leukocytosis (loo′-kō-sī-TŌ-sis), an increase in the number of WBCs above 10,000/μL,

A

is a normal protective response to stresses such as invading microbes, strenuous exercise, anesthesia, and surgery

182
Q

An abnormally low level of white blood cells (below 5000/μL) is termed

A

leukopenia (loo′-kō-PĒ-nē-a). It is never beneficial and may be caused by radiation, shock, and certain chemotherapeutic agents.

183
Q

Once pathogens enter the body, the general function of white blood cells is to

A

combat them by phagocytosis or immune responses

184
Q

many WBCs leave the bloodstream and

A

collect at sites of pathogen invasion or inflammation

185
Q

Once granular leukocytes and monocytes leave the bloodstream to fight injury or infection,

A

they never return to it.

186
Q

Lymphocytes continually

A

recirculate—from blood to interstitial spaces of tissues to lymph plasma and back to blood. Only 2% of the total lymphocyte population is circulating in the blood at any given time; the rest is in lymph plasma and organs such as the skin, lungs, lymph nodes, and spleen.

187
Q

WBCs leave the bloodstream by a process termed

A

emigration (em′-i-GRĀ-shun; e- = out; -migra- = wander), also called diapedesis (dī-a-pe-DĒ-sis), in which they roll along the endothelium, stick to it, and then squeeze between endothelial cells

188
Q

Molecules known as adhesion molecules

A

help WBCs stick to the endothelium.

189
Q

The shapes of their nuclei and the staining properties of their cytoplasmic granules

A

distinguish white blood cells from one another.

190
Q

Neutrophils and macrophages are active in

A

phagocytosis (fag′-ō-sī-TŌ-sis); they can ingest microbes and dispose of dead matter

191
Q

chemotaxis

A

When Several different chemicals released by microbes and inflamed tissues attract phagocytes

192
Q

Among WBCs, neutrophils respond

A

most quickly to tissue destruction by microbes

193
Q

After engulfing a pathogen during phagocytosis, a neutrophil

A

unleashes several chemicals to destroy the pathogen

194
Q

What chemicals does a neutrophil use to destroy pathogens

A

the enzyme lysozyme (LĪ-sō-zīm), which destroys certain bacteria, and strong oxidants, such as the superoxide anion (O2−), hydrogen peroxide (H2O2), and the hypochlorite anion (OCl−), which is similar to household bleach.

195
Q

Neutrophils also contain defensins which are

A

proteins that exhibit a broad range of antibiotic activity against bacteria and fungi

196
Q

Defensins form

A

peptide “spears” that poke holes in microbe membranes; the resulting loss of cellular contents kills the invader.

197
Q

Eosinophils

A

leave the capillaries and enter tissue fluid. They are believed to release enzymes, such as histaminase, that combat the effects of histamine and other substances involved in inflammation during allergic reactions. Eosinophils also phagocytize antigen–antibody complexes and are effective against certain parasitic worms. A high eosinophil count often indicates an allergic condition or a parasitic infection.

198
Q

At sites of inflammation, basophils

A

leave capillaries, enter tissues, and release granules that contain heparin, histamine, and serotonin. These substances intensify the inflammatory reaction and are involved in hypersensitivity (allergic) reactions.

199
Q

Like basophils, mast cells

A

release substances involved in inflammation, including heparin, histamine, and proteases.

200
Q

Most lymphocytes

A

continually move among lymphoid tissues, lymph plasma, and blood, spending only a few hours at a time in blood. Thus, only a small proportion of the total lymphocytes is present in the blood at any given time.

201
Q

Three main types of lymphocytes

A

are B cells, T cells, and natural killer cells.

202
Q

B cells are particularly effective in

A

destroying microbes and inactivating their toxins.

203
Q

T cells

A

attack infected body cells and tumor cells, and are responsible for the rejection of transplanted organs.

204
Q

Natural killer cells

A

attack a wide variety of infected body cells and certain tumor cells.

205
Q

Monocytes

A

take longer to reach a site of infection than neutrophils, but they arrive in larger numbers and destroy more microbes. On their arrival, monocytes enlarge and differentiate into wandering macrophages, which clean up cellular debris and microbes by phagocytosis after an infection.

206
Q

an increase in the number of circulating WBCs

A

usually indicates inflammation or infection.

207
Q

Because each type of white blood cell plays a different role

A

determining the percentage of each type in the blood assists in diagnosing the condition.

208
Q

High neutrophil counts may indicate

A

Bacterial infection, burns, stress, inflammation.

209
Q

Low neutrophil counts may indicate

A

Radiation exposure, drug toxicity, vitamin B12 deficiency, systemic lupus erythematosus.

210
Q

High lymphocyte counts may indicate

A

Viral infections, some leukemias, infectious mononucleosis.

211
Q

Low lymphocyte counts may indicate

A

Prolonged illness, HIV infection, immunosuppression, treatment with cortisol.

212
Q

High monocyte counts may indicate

A

Viral or fungal infections, tuberculosis, some leukemias, other chronic diseases.

213
Q

Low monocyte counts may indicate

A

Bone marrow suppression, treatment with cortisol.

214
Q

High eosinophil counts may indicate

A

Allergic reactions, parasitic infections, autoimmune diseases.

215
Q

Low eosinophils may indicate

A

Drug toxicity, stress, acute allergic reactions.

216
Q

High basophil counts may indicate

A

Allergic reactions, leukemias, cancers, hypothyroidism.

217
Q

Low basophil counts may indicate

A

Pregnancy, ovulation, stress, hypothyroidism.

218
Q

Besides the immature cell types that develop into erythrocytes and leukocytes, hemopoietic stem cells also differentiate into cells that produce

A

platelets

219
Q

Under the influence of the hormone thrombopoietin,

A

myeloid stem cells develop into megakaryocyte colony-forming cells that in turn develop into precursor cells called megakaryoblasts

220
Q

Megakaryoblasts transform into megakaryocytes wich are

A

huge cells that splinter into 2000 to 3000 fragments. Each fragment, enclosed by a piece of the plasma membrane, is a platelet

221
Q

Platelets break off from the megakaryocytes

A

in red bone marrow and then enter the blood circulation

222
Q

platelet granules contain chemicals that, once released,

A

promote blood clotting

223
Q

Platelets help stop blood loss from damaged blood vessels by

A

forming a platelet plug.

224
Q

Platelets have a short life span,

A

normally just 5 to 9 days. Aged and dead platelets are removed by fixed macrophages in the spleen and liver.

225
Q

Neutrophils constitute

A

60–70% of all WBCs.

226
Q

Describe a neutrophil

A

10–12 μm diameter; nucleus has 2–5 lobes connected by thin strands of chromatin; cytoplasm has very fine, pale lilac granules.

227
Q

What is the function of neutrophils

A

Phagocytosis. Destruction of bacteria with lysozyme, defensins, and strong oxidants, such as superoxide anion, hydrogen peroxide, and hypochlorite anion.

228
Q

Eosinophils constitute

A

2–4% of all WBCs.

229
Q

Describe eosinophils

A

10–12 μm diameter; nucleus usually has 2 lobes connected by thick strand of chromatin; large, red-orange granules fill cytoplasm.

230
Q

What is the function of eosinophils

A

Combat effects of histamine in allergic reactions, phagocytize antigen–antibody complexes, and destroy certain parasitic worms.

231
Q

Basophils constitute

A

0.5–1% of all WBCs.

232
Q

describe Basophils

A

8–10 μm diameter; nucleus has 2 lobes; large cytoplasmic granules appear deep blue-purple.

233
Q

What is the function of basophils

A

Liberate heparin, histamine, and serotonin in allergic reactions that intensify overall inflammatory response.

234
Q

Lymphocytes constitute

A

20–25% of all WBCs.

235
Q

Describe lymphocytes

A

Small lymphocytes are 6–9 μm in diameter; large lymphocytes are 10–14 μm in diameter; nucleus is round or slightly indented; cytoplasm forms rim around nucleus that looks sky blue; the larger the cell, the more cytoplasm is visible.

236
Q

what is the function of lymphocytes

A

Mediate immune responses, including antigen–antibody reactions. B cells develop into plasmocytes, which secrete antibodies. T cells attack invading viruses, cancer cells, and transplanted tissue cells. Natural killer cells attack wide variety of infectious microbes and certain spontaneously arising tumor cells.

237
Q

Monocytes constitute

A

3–8% of all WBCs.

238
Q

Describe monocytes

A

12–20 μm diameter; nucleus is kidney- or horseshoe-shaped; cytoplasm is blue-gray and appears foamy.

239
Q

What is the function of monocytes

A

Phagocytosis (after transforming into fixed or wandering macrophages).

240
Q

Describe platelets

A

2–4 μm diameter cell fragments that live for 5–9 days; contain many vesicles but no nucleus.

241
Q

What is the function of platelets

A

Form platelet plug in hemostasis; release chemicals that promote vascular spasm and blood clotting.

242
Q

A bone marrow transplant is

A

the replacement of cancerous or abnormal red bone marrow with healthy red bone marrow in order to establish normal blood cell counts

243
Q

In patients with cancer or certain genetic diseases in need of a red bone marrow transplant

A

the defective red bone marrow is destroyed by high doses of chemotherapy and whole body radiation just before the transplant takes place. These treatments kill the cancer cells and destroy the patient’s immune system in order to decrease the chance of transplant rejection.

244
Q

How does a red bone marrow transplant work

A

The red bone marrow from a donor is usually removed from the iliac crest of the hip bone under general anesthesia with a syringe and is then injected into the recipient’s vein, much like a blood transfusion.

245
Q

What happens after a patient is injected with a donor´s red bone marrow

A

The injected marrow migrates to the recipient’s red bone marrow cavities, where the donor’s stem cells multiply

246
Q

What is the u;timate goal of a bone marrow transplant

A

the recipient’s red bone marrow is replaced entirely by healthy, noncancerous cells.

247
Q

Bone marrow transplants have been used to treat

A

aplastic anemia, certain types of leukemia, severe combined immunodeficiency disease, Hodgkin’s disease, non-Hodgkin’s lymphoma, multiple myeloma, thalassemia, sickle-cell disease, breast cancer, ovarian cancer, testicular cancer, and hemolytic anemia

248
Q

After a bone marrow transplant there are some draw backs

A

Compromised immunity
Potential for donor cells to attack the patient or vice versa
Patients must take immunosuppresive drugs to prevent the hosts defenses from fighting donor cells which compromises immunity even more

249
Q

A more recent advance for obtaining stem cells involves

A

a cord-blood transplant.

250
Q

Stem cells from the cord have several advantages over those obtained from red bone marrow:

A

They are easily collected following permission of the newborn’s parents.
They are more abundant than stem cells in red bone marrow.
They are less likely to cause graft-versus-host disease, so the match between donor and recipient does not have to be as close as in a bone marrow transplant. This provides a larger number of potential donors.
They are less likely to transmit infections.
They can be stored indefinitely in cord-blood banks.

251
Q

Hemostasis (hē-mō-STĀ-sis), not to be confused with the very similar term homeostasis,

A

is a sequence of responses that stops bleeding.

252
Q

When blood vessels are damaged or ruptured, the hemostatic response must be

A

quick, localized to the region of damage, and carefully controlled in order to be effective.

253
Q

Three mechanisms reduce blood loss:

A

(1) vascular spasm, (2) platelet plug formation, and (3) blood clotting (coagulation).

254
Q

When successful, hemostasis prevents

A

hemorrhage (HEM-o-rij; -rhage = burst forth), the loss of a large amount of blood from the vessels.

255
Q

When arteries or arterioles are damaged,

A

the circularly arranged smooth muscle in their walls contracts immediately, a reaction called vascular spasm.

256
Q

What role does vascular spasm play in hemostasis

A

reduces blood loss for several minutes to several hours, during which time the other hemostatic mechanisms go into operation

257
Q

What causes vascular spasm

A

damage to the smooth muscle, by substances released from activated platelets, and by reflexes initiated by pain receptors.

258
Q

Considering their small size, platelets store an impressive array of chemicals. List them

A

Within many vesicles are clotting factors, ADP, ATP, Ca2+, and serotonin. Also present are enzymes that produce thromboxane A2, a prostaglandin; fibrin-stabilizing factor, which helps to strengthen a blood clot; lysosomes; some mitochondria; membrane systems that take up and store calcium and provide channels for release of the contents of granules; and glycogen

259
Q

Also within platelets is platelet-derived growth factor (PDGF) which is

A

a hormone that can cause proliferation of vascular endothelial cells, vascular smooth muscle fibers, and fibroblasts to help repair damaged blood vessel walls.

260
Q

What is the first step in platelet plug formation

A

Initially, platelets contact and stick to parts of a damaged blood vessel, such as collagen fibers of the connective tissue underlying the damaged endothelial cells. This process is called platelet adhesion.

261
Q

What is the second step in platelet plug formation

A

Due to adhesion, the platelets become activated, and their characteristics change dramatically. They extend many projections that enable them to contact and interact with one another, and they begin to liberate the contents of their vesicles. This phase is called the platelet release reaction. Liberated ADP and thromboxane A2 play a major role by activating nearby platelets. Serotonin and thromboxane A2 function as vasoconstrictors, causing and sustaining contraction of vascular smooth muscle, which decreases blood flow through the injured vessel.

262
Q

What is the third step in platelet plug formation

A

The release of ADP makes other platelets in the area sticky, and the stickiness of the newly recruited and activated platelets causes them to adhere to the originally activated platelets. This gathering of platelets is called platelet aggregation. Eventually, the accumulation and attachment of large numbers of platelets form a mass called a platelet plug.

263
Q

A platelet plug can .

A

stop blood loss completely if the hole in a blood vessel is small enough

264
Q

A platelet plug is very effective in

A

preventing blood loss in a small vessel

265
Q

A blood clot is

A

a gel that contains formed elements of the blood entangled in fibrin threads.

266
Q

blood serum, is

A

simply blood plasma minus the clotting proteins.

267
Q

A blood clot consists of

A

It consists of a network of insoluble protein fibers called fibrin in which the formed elements of blood are trapped

268
Q

The process of gel formation, called clotting or coagulation (kō-ag-u-LĀ-shun), is

A

a series of chemical reactions that culminates in formation of fibrin threads.

269
Q

If blood clots too easily, the result can be

A

thrombosis (throm-BŌ-sis; thromb- = clot; -osis = a condition of)—clotting in an undamaged blood vessel

270
Q

If the blood takes too long to clot,

A

hemorrhage can occur.

271
Q

Clotting involves several substances known as

A

clotting (coagulation) factors.

272
Q

Clotting factors include

A

calcium ions (Ca2+), several inactive enzymes that are synthesized by hepatocytes (liver cells) and released into the bloodstream, and various molecules associated with platelets or released by damaged tissues.

273
Q

Clotting is a complex cascade of

A

enzymatic reactions in which each clotting factor activates many molecules of the next one in a fixed sequence.

274
Q

What is the end product of clotting

A

a large quantity of product (the insoluble protein fibrin) is formed.

275
Q

What is the first stage of blood clotting

A

Two pathways, called the extrinsic pathway and the intrinsic pathway lead to the formation of prothrombinase. Once prothrombinase is formed, the steps involved in the next two stages of clotting are the same for both the extrinsic and intrinsic pathways, and together these two stages are referred to as the common pathway.

276
Q

What is the second stage in clotting

A

Prothrombinase converts prothrombin (a blood plasma protein formed by the liver) into the enzyme thrombin.

277
Q

What is the third stage of blood clotting

A

Thrombin converts soluble fibrinogen (another blood plasma protein formed by the liver) into insoluble fibrin. Fibrin forms the threads of the clot.

278
Q

The extrinsic pathway of blood clotting as opposed to the intrinsic pathway

A

has fewer steps than the intrinsic pathway and occurs rapidly—within a matter of seconds if trauma is severe

279
Q

The extrinsic pathway is so named because

A

a tissue protein called tissue factor (TF), also known as thromboplastin (throm′-bō-PLAS-tin), leaks into the blood from cells outside (extrinsic to) blood vessels and initiates the formation of prothrombinase.

280
Q

The abbreviation for tissue factor is

A

TF

281
Q

TF is

A

a complex mixture of lipoproteins and phospholipids released from the surfaces of damaged cells.

282
Q

In the presence of Ca2+, TF

A

begins a sequence of reactions that ultimately activates clotting factor X

283
Q

Once factor X is activated,

A

it combines with factor V in the presence of Ca2+ to form the active enzyme prothrombinase, completing the extrinsic pathway.

284
Q

The intrinsic pathway of blood clotting compared to the extrinsic pathway

A

is more complex than the extrinsic pathway, and it occurs more slowly, usually requiring several minutes

285
Q

The intrinsic pathway is so named because

A

its activators are either in direct contact with blood or contained within (intrinsic to) the blood; outside tissue damage is not needed

286
Q

If endothelial cells become roughened or damaged,

A

blood can come in contact with collagen fibers in the connective tissue around the endothelium of the blood vessel.

287
Q

trauma to endothelial cells causes

A

damage to platelets, resulting in the release of phospholipids by the platelets.

288
Q

Contact with collagen fibers (or with the glass sides of a blood collection tube)

A

activates clotting factor XII, which begins a sequence of reactions that eventually activates clotting factor X. Platelet phospholipids and Ca2+ can also participate in the activation of factor X

289
Q

Once factor X is activated

A

, it combines with factor V to form the active enzyme prothrombinase (just as occurs in the extrinsic pathway), completing the intrinsic pathway.

290
Q

In blood clotting, coagulation factors are activated

A

in sequence, resulting in a cascade of reactions that includes positive feedback cycles.

291
Q

The formation of prothrombinase marks the beginning of

A

the common pathway

292
Q

In the second stage of blood clotting

A

prothrombinase and Ca2+ catalyze the conversion of prothrombin to thrombin.

293
Q

In the third stage of blood clotting

A

, thrombin, in the presence of Ca2+, converts fibrinogen, which is soluble, to loose fibrin threads, which are insoluble. Thrombin also activates factor XIII (fibrin stabilizing factor), which strengthens and stabilizes the fibrin threads into a sturdy clot. Blood plasma contains some factor XIII, which is also released by platelets trapped in the clot.

294
Q

Thrombin has

A

two positive feedback effects.

295
Q

In the first Thrombin positive feedback loop, which involves factor V,

A

it accelerates the formation of prothrombinase. Prothrombinase in turn accelerates the production of more thrombin, and so on

296
Q

In the second Thrombin positive feedback loop

A

thrombin activates platelets, which reinforces their aggregation and the release of platelet phospholipids.

297
Q

Once a clot is formed,

A

it plugs the ruptured area of the blood vessel and thus stops blood loss.

298
Q

Clot retraction is

A

the consolidation or tightening of the fibrin clot.

299
Q

In clot retraction

A

The fibrin threads attached to the damaged surfaces of the blood vessel gradually contract as platelets pull on them. As the clot retracts, it pulls the edges of the damaged vessel closer together, decreasing the risk of further damage

300
Q

During retraction,

A

some blood serum can escape between the fibrin threads, but the formed elements in blood cannot.

301
Q

Normal retraction depends on

A

an adequate number of platelets in the clot, which release factor XIII and other factors, thereby strengthening and stabilizing the clot

302
Q

Once a clot is stabilized

A

Permanent repair of the blood vessel can then take place. In time, fibroblasts form connective tissue in the ruptured area, and new endothelial cells repair the vessel lining.

303
Q

Normal clotting depends on

A

adequate levels of vitamin K in the body.

304
Q

Although vitamin K is not involved in actual clot formation,

A

it is required for the synthesis of four clotting factors

305
Q

vitamin K is Normally produced

A

by bacteria that inhabit the large intestine, it is a fat-soluble vitamin that can be absorbed through the lining of the intestine and into the blood if absorption of lipids is normal.

306
Q

People suffering from disorders that slow absorption of lipids (for example, inadequate release of bile into the small intestine) often experience

A

uncontrolled bleeding as a consequence of vitamin K deficiency.

307
Q

Because blood clotting involves amplification and positive feedback cycles, a clot has a tendency to

A

enlarge, creating the potential for impairment of blood flow through undamaged vessels.

308
Q

The fibrinolytic system (fī-bri-nō-LIT-ik)

A

dissolves small, inappropriate clots; it also dissolves clots at a site of damage once the damage is repaired.

309
Q

Dissolution of a clot is called

A

fibrinolysis

310
Q

When a clot is formed,

A

an inactive blood plasma enzyme called plasminogen (plaz-MIN-o-jen) is incorporated into the clot.

311
Q

Both body tissues and blood contain substances that can activate plasminogen into

A

plasmin or fibrinolysin (fī-brin-ō-LĪ-sin), an active plasma enzyme.

312
Q

Among the substances that can activate plasminogen into plasmin are

A

thrombin, activated factor XII, and tissue plasminogen activator (t-PA), which is synthesized in endothelial cells of most tissues and liberated into the blood

313
Q

Once plasmin is formed, it can dissolve the clot by

A

digesting fibrin threads and inactivating substances such as fibrinogen, prothrombin, and factors V and XII.

314
Q

What is the common name for clotting factor I

A

Fibrinogen

315
Q

What is the source of fibrinogen

A

The Liver

316
Q

In what pathway of activation is Fibrinogen used

A

The common pathway

317
Q

What is the common name for clotting factor II

A

Prothrombin

318
Q

What is the source of prothrombin

A

the Liver

319
Q

In which pathway of activation is prothrombin used

A

The common pathway

320
Q

What is the common name for clotting factor III

A

Tissue factor (thromboplastin).

321
Q

What is the source of Tissue factor (thromboplastin).

A

Damaged tissues and activated platelets.

322
Q

In which pathway of activation is Tissue factor (thromboplastin) used

A

The extrinsic pathway

323
Q

What is the common name of clotting factor IV

A

Calcium ions (Ca2+).

324
Q

What is the source of Calcium ions

A

Diet, bones, and platelets.

325
Q

In what pathways of activation are calcium ions used

A

All pathways

326
Q

What is the common name for clotting factor V

A

Proaccelerin, labile factor, or accelerator globulin (AcG)

327
Q

What is the source of Proaccelerin, labile factor, or accelerator globulin (AcG)

A

The Liver and platelets.

328
Q

In what pathways of activation is clotting factor V used

A

Extrinsic and intrinsic pathways

329
Q

What is the common name for clotting factor VII

A

Blood serum prothrombin conversion accelerator (SPCA), stable factor, or proconvertin.

330
Q

What is the source of Blood serum prothrombin conversion accelerator (SPCA), stable factor, or proconvertin.

A

The Liver

331
Q

In what pathways of activation is clotting factor VII used

A

The extrinsic pathway

332
Q

What is the common name for clotting factor VIII

A

Antihemophilic factor (AHF), antihemophilic factor A, or antihemophilic globulin (AHG).

333
Q

What is the source of Antihemophilic factor (AHF), antihemophilic factor A, or antihemophilic globulin (AHG).

A

The Liver

334
Q

In what pathways of activation is clotting factor VIII used

A

intrinsic pathway

335
Q

What is the common name for clotting factor IX

A

Christmas factor, plasma thromboplastin component (PTC), or antihemophilic factor B.

336
Q

What is the source of Christmas factor, plasma thromboplastin component (PTC), or antihemophilic factor B.

A

The Liver

337
Q

In which pathways is clotting factor IX used

A

Intrinsic pathway

338
Q

What is the common name for clotting factor X

A

Stuart factor, Prower factor, or thrombokinase.

339
Q

What is the source of Stuart factor, Prower factor, or thrombokinase.

A

The Liver

340
Q

In what pathways is clotting factor X used in

A

intrinsic and extrinsic pathways

341
Q

What is the common name for clotting factor XI

A

Blood plasma thromboplastin antecedent (PTA) or antihemophilic factor C.

342
Q

What is the source of Blood plasma thromboplastin antecedent (PTA) or antihemophilic factor C.

A

The Liver

343
Q

in what pathways is clotting factor XI used

A

The intrinsic pathway

344
Q

What is the common name for clotting factor XII

A

Hageman factor, glass factor, contact factor, or antihemophilic factor D.

345
Q

What is the source of Hageman factor, glass factor, contact factor, or antihemophilic factor D.

A

The liver

346
Q

In what pathways of activation is clotting factor XII used

A

Intrinsic

347
Q

What is the common name for clotting factor XIII

A

Fibrin-stabilizing factor (FSF).

348
Q

What is the source of Fibrin-stabilizing factor (FSF).

A

Liver and platelets.

349
Q

In what pathways of activation is clotting factor XIII used

A

Common

350
Q

There is no factor

A

VI. Prothrombinase (prothrombin activator) is a combination of activated factors V and X.

351
Q

Even though thrombin has a positive feedback effect on blood clotting, clot formation normally

A

remains localized at the site of damage.

352
Q

A clot does not extend beyond a wound site into the general circulation,

A

because fibrin absorbs thrombin into the clot. Another reason for localized clot formation is that because of the dispersal of some of the clotting factors by the blood, their concentrations are not high enough to bring about widespread clotting.

353
Q

endothelial cells and white blood cells produce a prostaglandin called prostacyclin (pros-ta-SĪ-klin) that

A

opposes the actions of thromboxane A2. Prostacyclin is a powerful inhibitor of platelet adhesion and release.

354
Q

substances that delay, suppress, or prevent blood clotting, are

A

called anticoagulants (an′-tī-kō-AG-ū-lants), are present in blood.

355
Q

What are the three main anticoagulants

A

Antithrombin
Heparin
Activated protien C

356
Q

antithrombin function

A

blocks the action of several factors, including XII, X, and II (prothrombin)

357
Q

Heparin is

A

an anticoagulant that is produced by mast cells and basophils, combines with antithrombin and increases its effectiveness in blocking thrombin.

358
Q

activated protein C (APC),

A

inactivates the two major clotting factors not blocked by antithrombin and enhances activity of plasminogen activators.

359
Q

Despite the anticoagulating and fibrinolytic mechanisms,

A

blood clots sometimes form within the cardiovascular system.

360
Q

clots may be initiated by

A

roughened endothelial surfaces of a blood vessel resulting from atherosclerosis, trauma, or infection. These conditions induce adhesion of platelets

361
Q

Intravascular clots may form when

A

blood flows too slowly (stasis), allowing clotting factors to accumulate locally in high enough concentrations to initiate coagulation.

362
Q

thrombosis.

A

Clotting in an unbroken blood vessel (usually a vein)

363
Q

an intravascular clot is called a

A

thrombus

364
Q

A thrombus

A

may dissolve spontaneously.

365
Q

If a thrombus remains intact

A

the thrombus may become dislodged and be swept away in the blood

366
Q

embolus

A

A blood clot, bubble of air, fat from broken bones, or a piece of debris transported by the bloodstream

367
Q

An embolus that breaks away from an arterial wall may

A

lodge in a smaller-diameter artery downstream and block blood flow to a vital organ.

368
Q

pulmonary embolism.

A

When an embolus lodges in the lungs

369
Q

aspirin

A

inhibits vasoconstriction and platelet aggregation by blocking synthesis of thromboxane A2

370
Q

Thrombolytic agents (throm′-bō-LIT-ik) are

A

chemical substances that are injected into the body to dissolve blood clots that have already formed to restore circulation.

371
Q

The surfaces of erythrocytes contain

A

a genetically determined assortment of antigens composed of glycoproteins and glycolipids.

372
Q

Antigens on the surface of red blood cells are also called

A

agglutinogens

373
Q

Based on the presence or absence of various antigens,

A

blood is categorized into different blood groups.

374
Q

Within a given blood group,

A

there may be two or more different blood types

375
Q

There are at least __________ blood groups and more than __________ antigens that can be detected on the surface of red blood cells.

A

24
100

376
Q

The ABO blood group is based on

A

two glycolipid antigens called A and B

377
Q

People whose RBCs display only antigen A have

A

type A blood.

378
Q

Those who have only antigen B are

A

type B.

379
Q

Individuals who have both A and B antigens are

A

type AB

380
Q

those who have neither antigen A nor B are

A

type O.

381
Q

Blood plasma usually contains antibodies called agglutinins (a-GLOO-ti-nins) that

A

react with the A or B antigens if the two are mixed

382
Q

the anti A antibdy

A

reacts with antigen A,

383
Q

the anti-B antibody,

A

reacts with antigen B

384
Q

You do not have antibodies that react with

A

the antigens of your own RBCs

385
Q

you do have antibodies for

A

any antigens that your RBCs lack

386
Q

if your blood type is B, you have.

A

B antigens on your red blood cells, and you have anti-A antibodies in your blood plasma

387
Q

Because the antibodies are large IgM-type antibodies (see Table 22.3) that do not cross the placenta,

A

ABO incompatibility between a mother and her fetus rarely causes problems.

388
Q

A transfusion (trans-FŪ-zhun) is

A

the transfer of whole blood or blood components (red blood cells only or blood plasma only) into the bloodstream or directly into the red bone marrow.

389
Q

A transfusion is most often given to

A

alleviate anemia, to increase blood volume (for example, after a severe hemorrhage), or to improve immunity.

390
Q

In an incompatible blood transfusion,

A

antibodies in the recipient’s blood plasma bind to the antigens on the donated RBCs, which causes agglutination (a-gloo-ti-NĀ-shun), or clumping, of the RBCs.

391
Q

Agglutination is

A

an antigen–antibody response in which RBCs become cross-linked to one another.

392
Q

When antigen–antibody complexes form,

A

they activate blood plasma proteins of the complement family

393
Q

in an incompatible blood transfusion

A

complement molecules make the blood plasma membrane of the donated RBCs leaky, causing hemolysis (hē-MOL-i-sis) or rupture of the RBCs and the release of hemoglobin into the blood plasma The liberated hemoglobin may cause kidney damage by clogging the filtration membranes.

394
Q

The antibodies in your blood plasma

A

do not react with the antigens on your red blood cells.

395
Q

If the recipients antibodies bind to the antigens in the donors blood it is a worse condition because

A

the recipient has a large volume of blood with many antibodies that attach to donor blood

396
Q

If the antibodies in the donor´s blood bind to the antigens on the recipients blood the situation is

A

insignificant because the donors antibodies are diluted in te larger amount of blood volume in the recipient

397
Q

compatable donor blood types for a recipient with type A blood

A

A,O

398
Q

Compatable donor blood types for a recipient with type B blood

A

B,O

399
Q

Compatable donor blood types for a recipient with type AB blood

A

A,B,AB,O

400
Q

Compatable donor blood types for a recipient with type O blood

A

O

401
Q

Incompatable donor blood types for a recipient with type A blood

A

B,AB

402
Q

Incompatable donor blood types for a recipient with type B blood

A

A,AB

403
Q

Incompatable donor blood types for a recipient with type AB blood

A

There are no incompatable donor types because AB is a universal recipient

404
Q

Incompatable donor blood types for a recipient with type O blood

A

A,B,AB

405
Q

In practice, use of the terms universal recipient and universal donor is misleading and dangerous because

A

Blood contains antigens and antibodies other than those associated with the ABO system that can cause transfusion problems.

406
Q

The Rh blood group is so named because

A

the antigen was discovered in the blood of the Rhesus monkey.

407
Q

People whose RBCs have Rh antigens are designated ___________; those who lack Rh antigens are designated _________

A

Rh+
Rh-

408
Q

Normally, blood plasma does not contain

A

anti-Rh antibodies.

409
Q

If an Rh− person receives an Rh+ blood transfusion

A

the immune system starts to make anti-Rh antibodies that remain in the blood. If a second transfusion of Rh+ blood is given later, the previously formed anti-Rh antibodies cause agglutination and hemolysis of the RBCs in the donated blood, and a severe reaction may occur.

410
Q

To avoid blood-type mismatches,

A

laboratory technicians type the patient’s blood and then either cross-match it to potential donor blood or screen it for the presence of antibodies.

411
Q

if a small amount of Rh+ blood leaks from the fetus through the placenta into the bloodstream of an Rh− mother,

A

the mother will start to make anti-Rh antibodies.

412
Q

After a mother starts to make anti Rh antibodies if she gets pregnant again

A

If the fetus is Rh−, there is no problem, because Rh− blood does not have the Rh antigen. If the fetus is Rh+, however, agglutination and hemolysis brought on by fetal–maternal incompatibility may occur in the fetal blood.

413
Q

The most common problem with Rh incompatibility is

A

hemolytic disease of the newborn (HDN),

414
Q

In the procedure for determining Rh factor,

A

a drop of blood is mixed with antiserum containing antibodies that will agglutinate RBCs displaying Rh antigens. If the blood agglutinates, it is Rh+; no agglutination indicates Rh−.

415
Q

Anemia (a-NĒ-mē-a) is

A

a condition in which the oxygen-carrying capacity of blood is reduced due to a decreased number of RBCs or a decreased amount of hemoglobin

416
Q

Inadequate absorption of iron, excessive loss of iron, increased iron requirement, or insufficient intake of iron causes

A

iron-deficiency anemia, the most common type of anemia.

417
Q

Inadequate intake of vitamin B12 or folic acid causes

A

megaloblastic anemia, in which red bone marrow produces large, abnormal red blood cells (megaloblasts).

418
Q

Insufficient hemopoiesis resulting from an inability of the stomach to produce intrinsic factor, which is needed for absorption of vitamin B12 in the small intestine, causes

A

pernicious anemia.

419
Q

Excessive loss of RBCs through bleeding resulting from large wounds, stomach ulcers, or especially heavy menstruation leads to

A

hemorrhagic anemia.

420
Q

RBC plasma membranes rupture prematurely in

A

hemolytic anemia

421
Q

Deficient synthesis of hemoglobin occurs in

A

thalassemia (thal′-a-SĒ-mē-a), a group of hereditary hemolytic anemias.

422
Q

Destruction of red bone marrow results in

A

aplastic anemia

423
Q

The RBCs of a person with sickle cell disease (SCD)

A

contain Hb-S, an abnormal kind of hemoglobin.

424
Q

Hemophilia (hē-mō-FIL-ē-a; -philia = loving) is

A

an inherited deficiency of clotting in which bleeding may occur spontaneously or after only minor trauma.

425
Q

The term leukemia (loo-KĒ-mē-a; leuko- = white) refers to

A

a group of red bone marrow cancers in which abnormal white blood cells multiply uncontrollably.

426
Q

Lymphoblastic leukemia (lim-fō-BLAS-tik) involves

A

cells derived from lymphoid stem cells (lymphoblasts) and/or lymphocytes.

427
Q

Myelogenous leukemia (mī-e-LOJ-e-nus) involves

A

cells derived from myeloid stem cells (myeloblasts).

Bio 139 (4 decks)

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