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95 Cards in this Set

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BLOOD
liquid connective tissue
cells surrounded by liquid extracellular matrix.

Extracellular matrix = blood plasma
FUNCTIONS OF BLOOD: TRANSPORTATION
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
FUNCTIONS OF BLOOD: REGULATION
circulating blood maintain homeostasis of body fluids
regulate pH through buffers
adjust body temp through heat absorbing & coolant properties of blood plasma
FUNCTIONS OF BLOOD: PROTECTION
clots, prevents excessive loss of blood
WBC protect against disease by phagocytosis
blood proteins (antibodies) protect against disease
PHYSICAL CHARACTERISTICS OF BLOOD
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
COMPONENTS OF BLOOD
blood plasma + formed elements

45% formed elements, 55% blood plasma
more than 99% of formed elements are RBC WBC/platelets less than 1%
BLOOD PLASMA
91.5% water and 8.5% solutes, most plasma proteins

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

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

binds specifically to antigen that stimulated its production, disables invading antigen
FORMED ELEMENTS
red blood cells + white blood cells + platelets

types of WBC: neutrophils, lymphocytes, monocytes, eosinophils, basophils
HEMATOCRIT
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
AMENIA
significant drop in hematocrit
POLYCYTHEMIA
abnormally high level of RBCs
HEMOPOIESIS
process which formed elements of blood develop

primary site red bone marrow
RED BONE MARROW
highly vascularized connective tissue located in microscopic spaces between trabeculae of spongy bone tissue
PLURIPOTENT STEM CELLS
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
PROGENITOR CELLS
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
HEMOPOIETIC GROWTH FACTORS
several hormones regulate differentiation and proliferation of progenitor cells.
ERYTHROPOIETIN (EPO)
increases number of RBC precursors produced primarily by cells in kidneys that lie between kidney tubules.
THROMBOPOIETIN (TPO)
hormone produced by liver that stimulates formation of platelets from megakaryocytes
CYTOKINES
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
RED BLOOD CELLS / ERYTHROCYTES
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
RBC ANATOMY
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
HEMOGLOBIN
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
RBC LIFE CYCLE
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.
ERYTHROPOIESIS
prod of RBCs, starts in red bone marrow with precursor cell proerythroblast.

end of development sequence ejects nucleus, becomes reticulocyte
HYPOXIA
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
WBC / LEUKOCYTES
have nuclei and organelles, but no hemoglobin classified as either granular or agranular
GRANULAR LEUKOCYTES
neutrophils, eosinophils, basophils
NEUTROPHILS
small granules, evenly distributed, pale lilac, do not strongly attract either acidic (red) or basic (blue) stain
EOSINOPHILS
large, uniform sized granules, stain red-orange with acidic dyes
BASOPHIL
round, variable sized granules, stain blue-purple with basic dyes
AGRANULAR LEUKOCYTES
lymphocytes, monocytes
LYMPHOCYTES
nucleus stains dark, round/slightly indented; large & small lymphocyte
MONOCYTES
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
MAJOR HISTOCOMPABILITY (MHC) ANTIGENS
proteins, protruding from plasma membrane into ECF “cell identity markers”, unique for each person.
FUNCTIONS OF WBC
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
LEUKOCYTOSIS
increase # of WBCs above 10 000 microliters, normal protective response to stresses
LEUKPENIA
abnormally low level (below 5000).
CHEMOTAXIS
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
DIFFERENTIAL WHITE BLOOD CELL COUNT
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.
PLATELETS
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
HEMOSTASIS
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
VASCULAR SPASM
arteries or arterioles damaged, circularly arranged smooth muscle in walls contract immediately. Reduce blood loss for several minutes to hours.
PLATELET PLUG FORMATION
platelets store clotting factors, including ADP, ATP, calcium, serotonin, thromboxane A2. Fibrin, stabilizing factor (helps strengthen blood clot), lysosomes, glycogen
PLATELET PLUG FORMATION:
1. PLATELET ADHESION
platelets contact and stick to parts of damaged blood vessel, such as collagen fibers of connective tissue.
PLATELET PLUG FORMATION:
2. PLATELET RELEASE REACTION
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.
PLATELET PLUG FORMATION:
PLATELET AGGREGRATION
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.
SERUM
Straw coloured liquid, blood plasma without clotting proteins.
CLOT
Gel, consists of network of insoluble protein fibers called fibrin in which formed elements of blood are trapped.
CLOTTING / COAGULATION
Process of gel formation, series of chemical reactions that culminates in formation of fibrin threads.
THROMBOSIS
Blood clots too easily, results in clotting in undamaged blood vessel.
CLOTTING / COAGULATION FACTORS
calcium ions

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

various molecules associated with platelets or released by damaged tissues.
CLOTTING STAGES
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.
EXTRINSIC PATHWAY
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.
INTRINSIC PATHWAY
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.
COMMON PATHWAY
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.
CLOT RETRACTION
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.
VITAMIN K ROLE IN CLOTTING
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.
FIBRINOLYTIC SYSTEM
dissolves small, inappropriate clots; also dissolves clots at a site of damage once damage is repaired.
FIBRINOLYSIS
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.
ANTICOAGULANTS
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.
INTRAVASCULAR CLOTTING
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.
THROMBOSIS
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.
EMBOLUS
blood clot, bubble of air, fat from broken bones, or piece of debris transported by bloodstream
PULMONARY EMBOLISM
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.
ANTIGENS / AGGLUTINOGENS
composed of glycoproteins and glycolipids, genetically determined assortment on surface of erythrocytes.

occur in characteristic combinations
BLOOD GROUPS
Based on presence of antigens, blood is categorized by ---- .
BLOOD TYPES
Within a given blood group, there is 2 or more different ------.
ABO BLOOD GROUP
based on two glycolipid antigens called A & B.
TYPE A BLOOD
RBCs that display only antigen A
TYPE B BLOOD
RBCs that display only antigen B
TYPE AB BLOOD
Individuals with both A & B
TYPE O BLOOD
Those with neither antigen A or B
AGGLUTININS
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.
ANTI A ANTIBODY
reacts with antigen A
ANTI B ANTIBODY
reacts with antigen B
TRANSFUSIONS
transfer of whole blood or blood components into the bloodstream or directly into the red bone marrow.
AGGLUTINATION
incompatible blood transfusion, antibodies in recipient’s plasma bind to antigens on donated RBCs, cause clumping of RBCs.
HEMOLYSIS
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.
UNIVERSAL RECIPIENTS
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
UNIVERSAL DONORS
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.
Rh BLOOD GROUP
Rh antigen, first found on a Rhesus monkey.

RBCs have Rh antigens are Rh+ (Rh positive)
RBCs lack Rh antigens Rh- (Rh negative)
ANTI Rh ANTIBODIES
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.
HEMOLYTIC DISEASE OF NEWBORN (HDN)
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.
CROSS MATCHING BLOOD FOR TRANSFUSION
procedure for ABO blood typing, single drops of blood are mixed with different antisera, solutions that contain antibodies.
COMBINATIONS OF ANTI SERUM
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
Rh ANTI SERUM
drop of blood mixed with antiserum containing antibodies that will agglutinate RBCs displaying Rh antigens. If blood aggulinates, Rh+ ; no agglinate indicates Rh-
CROSS MATCH
possible donor RBCs mixed with recipients serum. If no agglutination occurs, recipient does not have antibodies that will attack donor RBCs.
ANEMIA
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.
SICKLE CELL DISEASE
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.
HEMOPHILIA
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.
LEUKEMIA
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
CYANOSIS
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.
JAUNDICE
abnormal yellowish discolouration of sclerae of the eyes, skin, and mucous membranes due to excess bilirubin (yellow-orange pigment) in the blood.
SEPTICEMIA
toxins or disease causing bacteria in the blood. “blood poisoning”