Chapter 19: The Blood

Front 1

BLOOD

Back 1

liquid connective tissue
cells surrounded by liquid extracellular matrix.

Extracellular matrix = blood plasma

Front 2

FUNCTIONS OF BLOOD: TRANSPORTATION

Back 2

oxygen from lungs to cells of body
CO2 from body cells to lungs (exhalation)
nutrients from GI tracts to body cell
hormones from endocrine glands to other body cells

Front 3

FUNCTIONS OF BLOOD: REGULATION

Back 3

circulating blood maintain homeostasis of body fluids
regulate pH through buffers
adjust body temp through heat absorbing & coolant properties of blood plasma

Front 4

FUNCTIONS OF BLOOD: PROTECTION

Back 4

clots, prevents excessive loss of blood
WBC protect against disease by phagocytosis
blood proteins (antibodies) protect against disease

Front 5

PHYSICAL CHARACTERISTICS OF BLOOD

Back 5

denser and more viscous than water, slightly sticky
around 38° C, pH 7.35 – 7.45

bright red - saturated with O2
dark red - unsaturated

20% ECF, 8% of total body mass, blood vol 5-6 L for males, 4-5 L for females

Front 6

COMPONENTS OF BLOOD

Back 6

blood plasma + formed elements

45% formed elements, 55% blood plasma
more than 99% of formed elements are RBC WBC/platelets less than 1%

Front 7

BLOOD PLASMA

Back 7

91.5% water and 8.5% solutes, most plasma proteins

hepatocytes (liver cells) synthesize plasma proteins:
-- albumins (54% of proteins)
-- globulins (38%)
-- fibrinogen (7%)

Front 8

ANTIBODIES / IMMUNOGLOBULINS

Back 8

plasma proteins

foreign substances (antigens) stimulate production of millions of different -----

binds specifically to antigen that stimulated its production, disables invading antigen

Front 9

FORMED ELEMENTS

Back 9

red blood cells + white blood cells + platelets

types of WBC: neutrophils, lymphocytes, monocytes, eosinophils, basophils

Front 10

HEMATOCRIT

Back 10

percentage of total blood volume occupied by RBC

avg for adult female = 38-46%
avg for adult male = 40-54%

testosterone stimulates synthesis of erythropoietin (EPO), in turn stimulates production of RBC

Front 11

AMENIA

Back 11

significant drop in hematocrit

Front 12

POLYCYTHEMIA

Back 12

abnormally high level of RBCs

Front 13

HEMOPOIESIS

Back 13

process which formed elements of blood develop

primary site red bone marrow

Front 14

RED BONE MARROW

Back 14

highly vascularized connective tissue located in microscopic spaces between trabeculae of spongy bone tissue

Front 15

PLURIPOTENT STEM CELLS

Back 15

red bone marrow cells derived from mesenchyme.

further divide into:
myeloid stem cells: give rise to RBCs, platelets, monocytes, neutrophils, eosinphils, basophils

lymphoid stem cells: give rise to lymphocytes

Front 16

PROGENITOR CELLS

Back 16

cannot reproduce themselves

give rise to more specific elements of blood, called colony forming units (CFU)
-- CFU-E: produce erythrocytes (RBC)
-- CFU-Meg: produce megakaryocytes (platelets)
-- CFU-GM: granulocytes (neutrophils), monocytes

Front 17

HEMOPOIETIC GROWTH FACTORS

Back 17

several hormones regulate differentiation and proliferation of progenitor cells.

Front 18

ERYTHROPOIETIN (EPO)

Back 18

increases number of RBC precursors produced primarily by cells in kidneys that lie between kidney tubules.

Front 19

THROMBOPOIETIN (TPO)

Back 19

hormone produced by liver that stimulates formation of platelets from megakaryocytes

Front 20

CYTOKINES

Back 20

small glycoproteins produced by red bone marrow cells, leukocytes, macrophages, fibroblasts, and endothelial cells.

Act as local hormones

Stimulate proliferation of progenitor cells in red bone marrow, regulate activities of cells involved in nonspecific defenses & immune responses.

2 families of cytokines that stimulate WBC formation:
• colony stimulating factors (CSF)
• interleukins

Front 21

RED BLOOD CELLS / ERYTHROCYTES

Back 21

contain oxygen carrying protein hemoglobin, pigment gives whole blood red colour.

adult male: 5.4 million RBC per microliter of blood
adult female: 4.8 million

new cells enter circulation at 2 million/sec

Front 22

RBC ANATOMY

Back 22

concave discs with diameter of 7-8 micrometers

plasma memb strong/flexible, stretch without rupturing

lack nucleus/organelles, cannot reproduce, carry extensive metabolic activities.

cytosol contains hemoglobin molecules

Front 23

HEMOGLOBIN

Back 23

protein globin composed of 4 polypeptide chains. ring-like nonprotein pigment heme bound to each chain

center of each ring iron ion, combine with O2, allows hemoglobin to bind 4 O2 molecules
-- transports 23% of total CO2

releases nitric oxide, causes vasodilation, increase in blood vessel diameter

Front 24

RBC LIFE CYCLE

Back 24

live about 120 days

ruptured RBC removed from circulation and destroyed by fixed phagocytic macrophages

iron removed from heme, in muscle fibers/liver cells iron attaches to iron-storage protein called ferritin.

Front 25

ERYTHROPOIESIS

Back 25

prod of RBCs, starts in red bone marrow with precursor cell proerythroblast.

end of development sequence ejects nucleus, becomes reticulocyte

Front 26

HYPOXIA

Back 26

cellular oxygen deficiency, occurs if too little oxygen enters blood

stimulates kidneys to step up release of erythropoietin, speeds development of proerythroblasts into reticulocytes;

# of RBC circulating increases = more O2 delivered to tissues

Front 27

WBC / LEUKOCYTES

Back 27

have nuclei and organelles, but no hemoglobin classified as either granular or agranular

Front 28

GRANULAR LEUKOCYTES

Back 28

neutrophils, eosinophils, basophils

Front 29

NEUTROPHILS

Back 29

small granules, evenly distributed, pale lilac, do not strongly attract either acidic (red) or basic (blue) stain

Front 30

EOSINOPHILS

Back 30

large, uniform sized granules, stain red-orange with acidic dyes

Front 31

BASOPHIL

Back 31

round, variable sized granules, stain blue-purple with basic dyes

Front 32

AGRANULAR LEUKOCYTES

Back 32

lymphocytes, monocytes

Front 33

LYMPHOCYTES

Back 33

nucleus stains dark, round/slightly indented; large & small lymphocyte

Front 34

MONOCYTES

Back 34

nucleus kidney shaped, cytoplasm blue-gray, foamy appearance.

Migrate from blood, enlarge and differentiate into macrophages; some become fixed (tissue) macrophages.

Wandering macrophages roam tissues and gather at sites of infection or inflammation

Front 35

MAJOR HISTOCOMPABILITY (MHC) ANTIGENS

Back 35

proteins, protruding from plasma membrane into ECF “cell identity markers”, unique for each person.

Front 36

FUNCTIONS OF WBC

Back 36

WBCs leave bloodstream, collect at sites of pathogen invasion, inflammation

granular leukocytes/monocytes leave bloodstream, never return; lymphocytes continually re-circulate

leave bloodstream by emigration, roll along endothelium, adhesion molecules help WBCs stick to endothelium

neutrophils/macrophages active in phagocytosis – ingest bacteria, dispose of dead matter

Front 37

LEUKOCYTOSIS

Back 37

increase # of WBCs above 10 000 microliters, normal protective response to stresses

Front 38

LEUKPENIA

Back 38

abnormally low level (below 5000).

Front 39

CHEMOTAXIS

Back 39

different chemicals released by microbes and inflamed tissues attract phagocytes

neutrophils respond quickly, engulfs pathogens then releases chemicals

eosinophils release enzymes such as histaminase to combat effects of histamine

3 main types of lymphocytes: B cells, T cells, natural killer cells

Front 40

DIFFERENTIAL WHITE BLOOD CELL COUNT

Back 40

count of each 5 types of WBCs to detect infection/inflammation; determine effects of possible poisoning by chemicals/drugs, monitor blood disorders, detect allergic reactions.

determine percentage of each type in blood assists in diagnosing condition.

Front 41

PLATELETS

Back 41

hemopoietic stem cells differentiate; under influence of hormone thrombopoietin, myeloid stem cells develop into precursor cells megakaryoblasts

cell splinters into 2000-3000 fragments, = -------

disc shaped, many vesicles but no nucleus
granules contain chemicals promote blood clotting, last 5-9 days

Front 42

HEMOSTASIS

Back 42

sequence of responses that stops bleeding

3 mechanisms: vascular spasm, platelet plug formation, blood clotting (coagulation)

prevents hemorrhage, loss of large amount of blood from vessels

Front 43

VASCULAR SPASM

Back 43

arteries or arterioles damaged, circularly arranged smooth muscle in walls contract immediately. Reduce blood loss for several minutes to hours.

Front 44

PLATELET PLUG FORMATION

Back 44

platelets store clotting factors, including ADP, ATP, calcium, serotonin, thromboxane A2. Fibrin, stabilizing factor (helps strengthen blood clot), lysosomes, glycogen

Front 45

PLATELET PLUG FORMATION:
1. PLATELET ADHESION

Back 45

platelets contact and stick to parts of damaged blood vessel, such as collagen fibers of connective tissue.

Front 46

PLATELET PLUG FORMATION:
2. PLATELET RELEASE REACTION

Back 46

platelets become activated, characteristics change extend projections enable them to contact and interact with one another, liberate contents of vesicles

serotonin and thromboxane A2 function as vasoconstrictors, causing contraction of vascular smooth muscle, decreases blood flow through injured vessel.

Front 47

PLATELET PLUG FORMATION:
PLATELET AGGREGRATION

Back 47

release of ADP makes other platelets in area sticky, causes them to adhere to originally activated platelets. Eventually accumulation and attachment of large numbers of platelets form a mass called platelet plug.

Front 48

SERUM

Back 48

Straw coloured liquid, blood plasma without clotting proteins.

Front 49

CLOT

Back 49

Gel, consists of network of insoluble protein fibers called fibrin in which formed elements of blood are trapped.

Front 50

CLOTTING / COAGULATION

Back 50

Process of gel formation, series of chemical reactions that culminates in formation of fibrin threads.

Front 51

THROMBOSIS

Back 51

Blood clots too easily, results in clotting in undamaged blood vessel.

Front 52

CLOTTING / COAGULATION FACTORS

Back 52

calcium ions

several inactive enzymes synthesized by hepatocytes (liver cells) and released into bloodstream,

various molecules associated with platelets or released by damaged tissues.

Front 53

CLOTTING STAGES

Back 53

extrinsic and intrinsic pathways lead to formation prothrombinase.

prothrombinase converts prothrombin (plasma protein) into enzyme thrombin.

thrombin converts soluble fibrinogen into insoluble fibrin; fibrin forms threads of clot.

Front 54

EXTRINSIC PATHWAY

Back 54

tissue protein, tissue factor (TF)/thromboplastin, leaks into blood from cells outside blood vessels and initiates formation of prothrombinase. TF complex mixture of lipoproteins and phospholipids release from surface of damaged cells.

Presence of calcium, TF begins sequence of reactions activates clotting factor X;

factor X activated, combines with factor V in presence of calcium ions to form active enzyme prothrombinase, completing pathway.

Front 55

INTRINSIC PATHWAY

Back 55

activators either in direct contact with blood or contained within the blood

contact with collagen fibers in connective tissue activates clotting factor XII, begins sequence of reactions eventually activates clotting factor X

platelet phospholipids and calcium ions can also participate in activation of factor X.

factor X activated, combines with factor V to form active enzyme prothrombinase, completing pathway.

Front 56

COMMON PATHWAY

Back 56

Beginning formation of prothrombinase

prothrombinase and calcium ions catalyze conversion of prothrombin to thrombin.

thrombin, in presence of calcium ions, converts fibrinogen which is soluble, to loose fibrin threads which are insoluble.

Also activates factor XIII (fibrin stabilizing factor) which strengthens and stabilizes fibrin threads into a sturdy clot.

Front 57

CLOT RETRACTION

Back 57

consolidation or tightening of fibrin clot. Fibrin threads attached to damaged surfaces of blood vessel gradually contract as platelets pull on them.

pulls on edges of damaged vessel closer together, decreasing risk of further damage.

Front 58

VITAMIN K ROLE IN CLOTTING

Back 58

required for synthesis of 4 clotting factors.

Produced by bacteria inhabit large intestine, absorbed through lining of intestine and into blood if absorption of lipids is normal.

Front 59

FIBRINOLYTIC SYSTEM

Back 59

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

Front 60

FIBRINOLYSIS

Back 60

dissolution of a clot

When clot formed, inactive plasma enzyme plasminogen, incorporated into clot. Both body tissues and blood contain substances that activate plasminogen to plasmin or fibrinolysin, an active plasma enzyme.

once plasmin formed, dissolve clot by digesting fibrin threads and inactivating substances such as fibrinogen, prothrombin, and factors V & XII.

Front 61

ANTICOAGULANTS

Back 61

substances that delay, suppress, or prevent blood clotting, present in blood.

include antithrombin, blocks action of factors including XII, X, & II

heparin, combines with antithrombin and increases effectiveness in blocking thrombin.

Front 62

INTRAVASCULAR CLOTTING

Back 62

clots form within cardiovascular system, can be initiated by roughened endothelial surfaces of blood vessel from atherosclerosis, trauma or infection; will induce adhesion of platelets

also form when blood flows too slowly, allowing clotting factors to accumulate locally in high enough concentrations to initiate coagulation.

Front 63

THROMBOSIS

Back 63

clotting in unbroken blood vessel (usually a vein)

clot itself thrombus, may dissolve spontaneously. If remains intact, thrombus may become dislodged and swept away in blood.

Front 64

EMBOLUS

Back 64

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

Front 65

PULMONARY EMBOLISM

Back 65

embolus breaks away from arterial wall may lodge in smaller diameter artery downstream and block blood flow to a vital organ; can lodge in lung.

Front 66

ANTIGENS / AGGLUTINOGENS

Back 66

composed of glycoproteins and glycolipids, genetically determined assortment on surface of erythrocytes.

occur in characteristic combinations

Front 67

BLOOD GROUPS

Back 67

Based on presence of antigens, blood is categorized by ---- .

Front 68

BLOOD TYPES

Back 68

Within a given blood group, there is 2 or more different ------.

Front 69

ABO BLOOD GROUP

Back 69

based on two glycolipid antigens called A & B.

Front 70

TYPE A BLOOD

Back 70

RBCs that display only antigen A

Front 71

TYPE B BLOOD

Back 71

RBCs that display only antigen B

Front 72

TYPE AB BLOOD

Back 72

Individuals with both A & B

Front 73

TYPE O BLOOD

Back 73

Those with neither antigen A or B

Front 74

AGGLUTININS

Back 74

antibodies in blood plasma that react with A or B antigens if the 2 are mixed.

Contain antibodies for any antigens RBCs lack.

Ex blood type B, you have B antigens on your RBCs, and you have anti-A antibody in your blood plasma.

Front 75

ANTI A ANTIBODY

Back 75

reacts with antigen A

Front 76

ANTI B ANTIBODY

Back 76

reacts with antigen B

Front 77

TRANSFUSIONS

Back 77

transfer of whole blood or blood components into the bloodstream or directly into the red bone marrow.

Front 78

AGGLUTINATION

Back 78

incompatible blood transfusion, antibodies in recipient’s plasma bind to antigens on donated RBCs, cause clumping of RBCs.

Front 79

HEMOLYSIS

Back 79

complement molecules make plasma membrane of the donated RBCs leaky = rupture of RBCs and release of hemoglobin into blood plasma.

Free hemoglobin can cause kidney damage by clogging filtration membranes.

Front 80

UNIVERSAL RECIPIENTS

Back 80

people with AB type blood do not have anti A or anti B antibodies in blood plasma, can receive blood from donors of all 4 types

Front 81

UNIVERSAL DONORS

Back 81

people with type O blood have neither A nor B antigens on RBCs, can donate blood to all 4 blood types.

Type O persons requiring blood can only receive type O blood.

Front 82

Rh BLOOD GROUP

Back 82

Rh antigen, first found on a Rhesus monkey.

RBCs have Rh antigens are Rh+ (Rh positive)
RBCs lack Rh antigens Rh- (Rh negative)

Front 83

ANTI Rh ANTIBODIES

Back 83

Blood plasma no anti-Rh antibodies; if Rh- person receives Rh+ transfusion, immune system will make anti-Rh antibodies that remain in blood.

If receive second transfusion, anti-Rh antibodies formed can cause aggulination and hemolysis.

Front 84

HEMOLYTIC DISEASE OF NEWBORN (HDN)

Back 84

can arise during pregnancy.

if small amount of Rh+ blood leaks from fetus into bloodstream of Rh- mother, mother start to make anti-Rh antibodies. During second pregnancy, anti-Rh antibodies cross placenta and enter bloodstream of fetus.

fetus is Rh+, aggulination and hemolysis brought on by fetal-maternal incompatibility may occur in fetal blood.

Front 85

CROSS MATCHING BLOOD FOR TRANSFUSION

Back 85

procedure for ABO blood typing, single drops of blood are mixed with different antisera, solutions that contain antibodies.

Front 86

COMBINATIONS OF ANTI SERUM

Back 86

One drop mixed with anti A serum (contains anti A antibodies), another mixed with anti B serum (contains anti B antibodies).

If RBC agglutinate only when mixed with anti-A serum, blood is type A

if RBC agglutinate only when mixed with anti B serum blood type B

If both drops agglutinate, blood type AB

If neither agglutinates, blood type O

Front 87

Rh ANTI SERUM

Back 87

drop of blood mixed with antiserum containing antibodies that will agglutinate RBCs displaying Rh antigens. If blood aggulinates, Rh+ ; no agglinate indicates Rh-

Front 88

CROSS MATCH

Back 88

possible donor RBCs mixed with recipients serum. If no agglutination occurs, recipient does not have antibodies that will attack donor RBCs.

Front 89

ANEMIA

Back 89

Condition which oxygen carrying capacity of blood reduced. All types characterized by reduced numbers of RBCs or decreased amount of hemoglobin in blood.

Person feels fatigued and intolerant of cold, skin appears pale, due to low content of red coloured hemoglobin circulating in blood vessels.

iron deficiency – inadequate absorption of iron, excessive iron loss, or insufficient intake of iron.

Megaloblastic anemia – inadequate intake of vitamin b12 or folic acid.

Hemorrhagic anemia results from excessive loss of RBCs through bleeding.

Front 90

SICKLE CELL DISEASE

Back 90

RBCs contain Hb-S, abnormal kind of hemoglobin. Hb-S gives up O2 to interstitial fluid, forms long stiff structures that bend erythrocyte into sickle shape, rupture easily.

RBCs break down prematurely, leading to anemia, shortness of breath, fatigue, paleness, and delayed growth and development in children.

stick together and form clumps that cause blockages in blood vessels.

Inherited, people with 2 sickle cell genes have severe anemia, those with only one defective gene have sickle cell trait.

Front 91

HEMOPHILIA

Back 91

Inherited deficiency in clotting, bleeding may occur spontaneously or after only minor trauma.

Different types due to deficiencies of different blood clotting factors and exhibit varying degrees of severity, ranging from mild to severe bleeding tendencies.

Characterized by spontaneous or traumatic subcutaneous and intramuscular hemorrhaging, nosebleeds, blood in the urine, and hemorrhages in joints that produce pain and tissue damage.

Front 92

LEUKEMIA

Back 92

Group of red bone marrow cancers which abnormal white blood cells multiply uncontrollably.

Accumulation of cancerous WBC in red bone marrow interferes with production of RBC, WBC and platelets. Result oxygen carrying capacity of blood is reduced, more susceptible to infection and blood clotting is abnormal.

Lymphoblastic leukemia involves cells derived from lymphoid stem cells and or lymphocytes

Myelogenous leukemia involves cells derived from myeloid stem cells.

Classified as acute (symptoms develop rapidly) or chronic

Front 93

CYANOSIS

Back 93

slightly bluish/purple skin discolouration, most easily seen in the nail beds and mucous membranes, due to increased quantity in methemoglobin, hemoglobin not combined with oxygen in systematic blood.

Front 94

JAUNDICE

Back 94

abnormal yellowish discolouration of sclerae of the eyes, skin, and mucous membranes due to excess bilirubin (yellow-orange pigment) in the blood.

Front 95

SEPTICEMIA

Back 95

toxins or disease causing bacteria in the blood. “blood poisoning”