Name: ___KEY____13.75 points_____________________________________ Period: ____ Chapter 14: THE CARDIOVASCULAR SYSTEM-BLOODI. FUNCTIONS OF BLOOD- page 350 8 questions @ 1/8 each = 1 point

OBJ: List and describe the functions of blood.Blood is liquid connective tissue.Three general functions:(1) _TRANSPORTATION_

a. Transports: _OXYGEN_, _CARBON DIOXIDE_, _NUTRIENTS_, _HEAT AND WASTE_, and _HORMONES_.

(2) _REGULATION_a. Helps to regulate: _pH_, _BODY TEMPERATURE_, and _WATER CONTENT _ of cells.

(3) _PROTECTION_a. Prevents: _BLOOD LOSS THROUGH CLOTTING_.b. Combats: _MICROBES_ and _TOXINS_ through action of certain phagocytic white blood cells

or specialized plasma proteins.c. _INTERFERONS_ and _COMPLEMENT_ are proteins that helps protect against disease.

II. COMPONENTS OF WHOLE BLOOD- pages 350-357 9 questions @ 1/8 each = 1 1/8 pointsOBJ: Discuss the formation, components, and functions of whole blood.Physical characteristics:Viscosity (stickiness) is greater than that of _WATER_.Temperature: _38_C or _100.4_F.pH range between _7.35_ and _7.45_. Is this alkaline or acidic? _SLIGHTLY ALKALINE__8_% of total body weight.Volume in average-sized adult male body = _5_ to _6_ liters or _1.5_gallons.Volume in average-sized adult female body = _4_ to _5_ liters or _1.2_gallons.Whole blood composed of two portions: (1) 55% _BLOOD PLASMA_ Liquid containing dissolved substances(2) 45% _FORMED ELEMENTS_ Cells and cell fragmentsHematocrit: _PERCENTAGE OF TOTAL BLOOD VOLUME OCCUPIED BY RED BLOOD CELLS_(3) Buffy coat: _THIN LAYER OF PLATELETS AND PALE COLORLESS WHITE BLOOD CELLS; LESS THAN 1% OF BLOOD VOLUME_

III. Blood Plasma- page 350 10 questions @ 1/8 each = 1 ¼ pointsComposition:a. 91.5 % _WATER_b. 7% _PROTEINS_c. 1.5% _SOLUTES_Principle solutes include:a. _PROTEINS ____________________ Examples: _ALBUMINS, GLOBULINS, FIBRINOGEN_b. _NUTRIENTS_c. _HORMONES_d. _RESPIRATORY GASES_e. _ELECTROLYTES_f. _WASTE PRODUCTS_

A. Formed Elements- pages 350-357 I. Red Blood CellsII. White Blood Cells

A. Granular leucocytes1. Neutrophils2. Eosinophils3. basophils

B. Agranular leucocytes1. T and B lymphocytes and natural killer cells2. Monocytes

III. Platelets1. Formation of Blood Cells- pages 353-355 10 question @ 1/8 each = 1 ¼ points

a. Hemopoiesis: _PROCESS BY WHICH THE FORMED ELEMENTS OF BLOOD DEVELOP FROM PLURIPOTENT STEM CELLS_

b. Occurs in: _RED BONE MARROW_

c. Where does hemopoiesis occur before birth? _YOLK SAC OF AN EMBRYO_d. Where does it occur in a fetus? _LIVER, SPLEEN, THYMUS, AND LYMPH NODES_e. Where does it occur during the last three months before birth? _RED BONE MARROW_f. After birth? _RED BONE MARROW_g. Red bone marrow is derived from mesenchymal cells called _PLURIPOTENT STEM CELLSh. When pluripotent stem cells are stimulated by specific hormones, they generate two

other types of stem cells: _MYELOID STEM CELLS_ and _LYMPHOID STEM CELLS_.i. Myeloid stem cells differentiate into _RED BLOOD CELLS_, _PLATELETS_,

_EOSINOPHILS_, _BASOPHILS_, _NEUTROPHILS_, and _MONOCYTES_.j. Lymphoid stem cells differentiate into _T_ and _B_ lymphocytes.

2. Red Blood Cells(RBCs)-PAGE 353 11 questions @ 1/8 each =1 3/8 pointsa. Also called _ERYTHROCYTES_b. Hemoglobin _OXYGEN-CARRYING PIGMENT_c. Hemoglobin gives whole blood its _RED COLOR_d. STRUCTURE OF RBCs:

_BICONCAVE DISCS_(concave on both sides)Average size: _7-9_µm in diameter 1µm = 1/25,000 OF AN INCHNo _NUCLEI_ or other _ORGANELLES_They _CANNOT_divide or _CARRY ON EXTENSIVE METABOLIC ACTIVITY_Only composed of : _SELECTIVELY PERMEABLE PLASMA MEMBRANE_, _CYTOSOL_, and_HEMOGLOBIN_.Healthy male has about _5.4_ million RBCs/µL of bloodHealthy female has about _4.8_ million RBCs/µL of blood

e. RBC LIFE CYCLE-PAGE 354 7 questions @ 1/4 each = 1 ¾ pointsLive about _120_days

f. Process for removing worn-out red blood cells from circulation:(1) _MACROPHAGES_ in spleen, liver, and red bone marrow through the process of

_PHAGOCYTOSIS_ rupture worn-out red blood cells splitting apart the _GLOBIN_ and _HEME_ portions of hemoglobin.

(2) Globin broken down into _AMINO ACIDS_ (to be used in protein synthesis).(3) _IRON_ removed from heme portion associates with plasma protein called

_TRANSFERRIN_.(4) _IRON-TRANSFERRIN COMPLEX_ goes to red bone marrow for RBC precursor cells to

use in hemoglobin synthesis.IRON NEEDED FOR HEME PORTION OF HEMOGLOBIN, AMINO ACID NEEDED FOR GLOBIN.Also needed: _VITAMIN B12_ and _INTRINSIC FACTOR_.

(5) _ERYTHROPOIESIS_ is the process in red bone marrow that results in production of new _RED BLOOD CELLS_.

(6) Iron removed from heme, non-iron portion converted to _BILIVERDIN_, a green pigment, and then into _BILIRUBIN_, a yellow-orange pigment. _BILIRUBIN_ enters

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OBTAIN A WORKSHEET OF RED BLOOD CELLS THAT SUMMARIZES THEIR FORMATION

blood and is transported to the _LIVER_, where it is secreted into _BILE_. Bile goes to small intestine then large intestine.

(7) Bacteria in large intestine converts bilirubin into _UROBILINOGEN_, which is absorbed back into the blood, and converted to a yellow pigment called _UROBILIN_, which is excreted in urine. Urobilinogen is eliminated in _FECES_ in the form of a brown pigment called _STERCOBILIN_.

g. RBC PRODUCTION-PAGE 355 6 questions @ 1/8 each = 3/4 point Erythropoiesis _FORMATION OF ONLY NEW RBCs IN THE RED BONE MARROW OF

ADULTS_h. RBC precursor ejects its nucleus becomes _A RETICULOCYTE_, center now indents.

BICONCAVE SHAPE…These leave red bone marrow and enter _BLOOD STREAM_.RETICULOCYTES ~ 34% HEMOGLOBIN RETAIN SOME MITOCHONDRIA, RIBOSOMES, AND ER UNTIL MATURE; MATURE IN 1-2 DAYS.RETOCULOCYE COUNT DIAGNOSTIC TEST THAT INDICATES THE RATE OR ERYTHROPOIESISi. Hypoxia _DEFICIENCY OF OXYGEN_NORMALLY ERYTHROPOIESIS AND DESCTRUCTION OF RBCs PROCEED AT SAME PACE…IF OXYGEN-CARRYING CAPACITY OF BLOOD FALLS BECAUSE ERYTHROPOIESIS FAILS TO KEEP UP WITH RBCs DESTRUCTION; ERYTHROCYTE PRODUCTION INCREASES = NEGATIVE FEEDBACK LOOP; KIDNEYS OXYGEN DELIVER AFFECTED / DEFICIENCY STIMULATES RELEASE OF ERYTHROPOIETIN OF ‘EPO’ (HORMONE MADE BY KIDNEYS)j. What does hypoxia stimulate? _THE RELEASE OF ERYTHROPOIETIN BY THE KIDNEYS_k. What does EPO do? _CIRCULATES THROUGH BLOOD TO RED BONE MARROW,

STIMULATES ERYTHROPOIESIS/ MORE RBCs PRODUCED MEANS MORE OXYGEN AVAILABLE_

‘ANEMIA’ LOWER THAN NORMAL NUMBER OF RBCs‘CYANOSIS’ IS PROLONGED HYPOXIA

3. White Blood Cells 6 questions @ 1/8 each =3/4 pointa. WBC STRUCTURE AND TYPES

Also called: _LEUKOCYTES_Have _NUCLEI_ but do not contain _HEMOGLOBIN_Classified as _GRANULAR_ or _AGRANULAR_ depending on whether or not they contain granules.Granular leukocytes include: _NEUTROPHILS_ _EOSINOPHILS_

_BASOPHILS_Agranular leukocytes include: _MONOCYTES AND LYMPHOCYTES_Three types OF LYMPHOCYTES: _B CELLS_, _T CELLS_, and_NATURAL KILLER CELLS_

b. WBC FUNCTIONS 3 questions @ 1/8 each =3/8 pointMain function: _COMBAT INFLAMMATION AND INFECTION_ Through process of : _PHAGOCYTOSIS_ Or through: _ANTIBODY PRODUCTION_NEUTROPHILS AND MACROPHAGES (WHICH DEVELOP FROM MONOCYTES) COMBAT INFECTION THEORUGH PHAGOCYTOSISEOSINOPHILS COMBAT INFLAMMATION IN ALLEGRIC REACTIONS; PHAGOCYTIZE ANTIGEN-ANTIBODY COMPLEXES, COMBAT PARASITE WORMSBASOPHILS LIBERATE HEPARIN (prevent blood clotting) , HISTAMINE (stimulates gastric secretion and causes dilation of capillaries, constriction of bronchial smooth muscle, and decreased blood pressure), AND SEROTONIN (include sleep, temperature regulation, sexual behaviour, appetite, learning, memory, endocrinal functions, anxiety, depression, moods, muscular functions

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as well as cardiovascular functions ) IN ALLEGERIC REACTIONS TO INTENSIFY INFLAMMATORY RESPONSEB CELLS EFFECTIVE AGAINST BACTERIA AND OTHER TOXINST CELLS AGAINST VIRUSES, FUNGI, AND CANCER CELLSNATURAL KILLER CELLS ATTACK MICROBES AND TUMOR CELLS

c. WBC LIFE SPAN 2 questions @ 1/8 each = 1/4 pointLife span = _FEW HOURS_ to a _FEW DAYS_Why??? Can phagocytize only a certain amount of bacteria before interferes with WBC metabolic activitiesNormal blood contains _5000_ to _10,000_ WBCs per µLLEUKOCYTOSIS = INCREASE IN NUMBER OF WBCs IN NORMAL, PROTECTIVE RESPONSE TO STRESSES: MICROBE INVADERS, STRENUOUS ACTIVITY, ANESTHESIA, AND SURGERY. USUALLY INDICATES INFECTION OR INFLAMMATIONDIFFERENTIAL WHITE BLOOD CELL COUNT, COUNTING DIFFERENT WBCs PRESENT SINCE DIFFERENT ONES COMBAT DIFFERENT THINGS CAN HELP AS A DIAGNOSTIC TOOLLEUKOPENIAABNORMALLY LOW LEVEL OF WBCs; never beneficial, causes may be exposure to radiation, shock, and certain chemotherapy agents

d. WBC PRODUCTION 3 questions @ 1/8 each =3/8 pointDeveloped in red bone marrow _LEUKOCYTES_Monocytes and granular leukocytes develop from _MYELOID STEM CELLS_T and B cells develop from _LYMPHOID TEM CELLS_

4. Platelets 4 questions @ 1/8 each =1/2 pointAre derived from: _PLURIPOTENT STEM CELLS_How platelets form: SOME MYELOID STEM CELLS DEVELOP INTO CELLS CALLED MEGAKARYOBLASTS, THESE SPLINTER INTO 2000-3000 FRAGMENTS IN RED BONE MARROW AND THEN ENTER BLOODSTREAMPlatelets help stop blood loss when blood vessels damaged by forming platelet plug; their vesicles promote blood clottingLife span 5-9 days; removed by macrophage in spleen and liverStructure: _DISK-SHAPED FRAGMENT________________________Lack a _NUCLEUS_Normal blood contains _250,000_ to _400,000_ platelets/µL

Table answers = 48 @ 1/16 each = 3 points

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Complete the ‘Comparison of RBCs, WBCs, and Platelets’ chart on the back of this page. Table14.2 on page 358 will help.

COM

PA

RIO

SN O

F R

BCs

, WB

Cs, A

ND

PLA

TEL

ETS

WH

ERE

FOR

MED

Red

bone

m

arro

w;

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stem

Red

bone

m

arro

w;

mye

loid

stem

Red

bone

m

arro

w;

mye

loid

stem

Red

bone

m

arro

w;

mye

loid

stem

Red

bone

m

arro

w;

mye

loid

stem

Red

bone

m

arro

w;

mye

loid

stem

Red

bone

m

arro

w;

lym

phoi

d st

em

LIFE

SP

AN

120

days

5-9

days

Few

hou

rs

to d

ays

Few

hou

rs

to d

ays

Few

hou

rs

to d

ays

Few

hou

rs

to d

ays

Few

hou

rs

to d

ays

Few

hou

rs

to d

ays

HEM

OG

LOB

IN?

YES

OR

NO

YES

NO

NO

NO

NO

NO

NO

NO

NU

CLEI

?Y

ES O

R N

O

NO

NO

YES

2-3

LOBE

S

YES

2 LO

BES

YES

2-5

LOBE

S

YES;

Kid

ney

or

hors

esho

e -

shap

ed

YES;

Lar

ge ro

und

& sl

ight

ly

inde

nted

DR

AW

ING

NU

MB

ERP

ER

µL

4.8

(fem

ale)

-5.4

(mal

e) m

illio

n RB

C

150,

000-

400

,00

~225

2-4%

of a

ll W

BCs

~75

0.5-

1% o

f all

WBC

s

~450

0

60-7

0% o

f all

WBC

~525

3-8%

of a

ll W

BCs

~100

0-15

00

20-2

5% o

f all

WBC

s

FUN

CTIO

N

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y O

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CO

2 (h

emog

lobi

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Form

plu

g to

stop

bl

ood

loss

; pr

omot

e cl

otting

Com

bat

effec

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of h

istam

ine;

de

stro

y pa

rasit

e w

orm

s

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rate

hep

arin

, hi

stam

ine,

&

sero

toni

n;

inte

nsify

in

flam

mat

ory

resp

iratio

n

Phag

ocyt

osis

dest

roy

bact

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Phag

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osis

beco

me

mac

roph

ages

Attac

k in

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ance

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tran

spla

nt ti

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ce

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me

plas

ma

cells

& se

cret

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tibod

ies

TY

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OF

CELL

Eryt

hroc

ytes

Plat

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Baso

phils

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hils

Mon

ocyt

es

T ce

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5

Name: _KEY_____15 POINTS________________________________ Period: _____IV. HEMOSTASIS- pages 357-362

OBJ: Describe the various mechanisms that prevent blood loss.Hemostasis _SEQUENCE OF RESPONSES THAT STOPS BLEEDING WHEN BLOOD VESSELS ARE INJURED__1/4 POINT_Three mechanisms that reduce blood loss: 1/4 POINT(1) _VASCULAR SPASM__________________________________(2) _PLATELET PLUG FORMATION_________________________(3) _ BLOOD CLOTTING (COAGULATION)____________________When hemostasis is successful what condition is averted? _HEMORRHAGE__1/4 POINT _From what type of vessels? _SMALLER BLOOD VESSELS__1/4 POINT _A. Vascular Spasm- read page 359 and complete the questions below

1. What occurs during a vascular spasm response? _BLOOD VESSEL DAMAGES; SMOOTH MUSCLE IN ITS WALL CONTRACTS IMMEDIATELY_1/4 POINT

2. What do vascular spasm reduce and for how long? _BLOOD LOSS FOR SEVERAL MINUTES TO A FEW HOURS_1/4 POINT

3. What is vasoconstriction? _NARROWING OF THE BLOOD VESSEL; PLATELETS ACCUMULATE AT DAMAGE SITE-RELEASE CHEMICALS TO ENHANCE VASOCONSTRICTION- MAINTAINS VASCULAR SPASM_ 1/4 POINT

B. Platelet Plug Formation- read page 359 and complete the questions below1. How are platelet plugs formed? _BY PLATELETS COMING INTO CONTACT WITH PARTS OF A

DAMAGED BLOOD VESSEL THEY CHANGE DRASTICALLY AND COME TOGETHER TO FORM A PLATELET PLUG_1/4 POINT

2. List the name of each process and briefly explain what is taking place in each of the diagrams below:a. _PLATELET ADHESION_

_PLATELETES CONTACT AND STICK TO PARTS OF DAMAGED BLOOD VESSEL; I.E. TO COLLAGEN FIBERS OF THE CONNECTIVE TISSUE UNDERLYING DAMAGED ENDOTHELIAL CELLS_1/4 POINT

b. _PLATELET RELEASE REACTION__RESULT OF ADHESION = PLATELETS ACTIVATED, THEIR CHARACTERISTICS CHANGE, THEY EXTEND MANY PROJECTIONS THAT ENABLE THEM TO CONTACT AND INTERACT WITH ONE ANOTHER, THEY BEGIN TO LIBERATE THE CHEMICALS CONTAINED IN THEIR VESICLES. LIBERATED CHEMICALS ACTIVATE NEARBY PLATELETS AND SUSTAIN VASCULAR SPASM, THUS DECRESING BLOOD FLOW THROUGH INJURED BLOOD VESSEL._ 1/4 POINT

c. _PLATELET AGGREGATION__RELEASE OF CEHEMICALS MAKES PLATELETS IN THE AREA STICKY, THEY IN TURN STICK TO THE ORIGINALLY ACTIVATED PLATELETS; GATHERING OF PLATELETS= PLATLET AGGREGATION. EVENTUALKY THEY FORM A MASS CALLED A PLATELET PLUG; IT STOPS BLOOD LOSS COMPLETELY IF HOLE IN BLOOD VESSEL SMALL ENOUGH_1/4 POINT

C. Clotting- read pages 359-361 and complete the questions belowWhat is serum? _PLASMA MINUS CLOTTING PROTEINS_1/2 POINTWhat is a clot composed of? _A NETWORK OF INSOLUBLE PROTEIN FIBERS CALLED FIBRIN FILLED WITH TRAPPED FORMED ELEMENTS_1/2 POINTWhat is clotting or coagulation? _SERIES OF CHEIMCAL REACTIONS THAT CULMINATES IN THE FORMATION OF FIBRIN THREADS_1/2 POINT

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How does thrombosis occur? _IF BLOOD CLOTS TOO EASILY; RESULT = CLOTTING IN AN UNBROKEN BLOOD VESSEL_1/2 POINTHow does hemorrhage occur? _ IF BLOOD TAKES TOO LONG TO CLOT; RESULT = UNCONTROLLED ENORMOUS LOSS OF BLOOD_1/2 POINTRefer to the diagram below and briefly explain in your own words the three stages of the clotting process below: CLOTTING FACTORS: CALCIUM IONS, ENZYMES, AND MOLECULES ASSOCIATED WITH PLATELETS OR DAMAGED TISSUES ACTIVATE EACH OTHER DURING THE CLOTTING PROCESS…(1) _PROTHROMBINASE IS FORMED_1/3 POINT(2) _THE CONVERTED TO PROTHROMBIN (PLASMA PROTEIN FORMED BY LIVER WITH HELP OF

VITAMIN K); NEXT CONVERTED TO ENZYME THROMBIN_1/3 POINT(3) _THROMBIN CONVERTS SOLUBLE FIBRINOGEN (PLASMA PROTEIN FORMED BY LIVER) INTO

SOLUBLE FIBRIN; FIBRIN FORMS THREADS OF CLOT_1/3 POINT

Explain the differences between the extrinsic pathway and intrinsic pathway of blood clotting for forming prothrombinase. _EXTRINSIC PATHWAY: OCCURS RAPIDLY WITHIN SECONDS. DAMAGED TISSUE CELLS RELEASE TISSUE PROTEIN CALLED TISSUE FACTOR (TF) INTO BLOOD OUTSIDE (EXTRINSIC) TO BLOOD VESSELS. ADDITIONAL REACTIONS THAT REQUIRE CALCIUM AND SEVERAL CLOTTING FACTORS FOLLOW, AND TISSUE FACTOR IS CONVERTED INTO PROTHROMBINASE…_1 POINT_INTRINSIC PATHWAY: OCCURS MORE SLOWLY (REQUIRES SEVERAL MINUTES); ACTIVATORS ARE EITHER IN DIRECT CONTACT WITH BLOOD OR CONTAINED WITHIN BLOOD; TAKE PLACE ON ACTIVATED PLATELETS. ADDITIONAL REACTIONS THAT REQUIRE CALCIUM AND SEVERAL CLOTTING FACTORS FOLLOW, AND PROTHROMBINASE ACTIVITY OCCURS ON THE PLATELETS._ 1 POINT1. Clear Retraction and Blood Vessel Repair

What is a clot retraction? _CONSOLIDATON OR TIGHTENING OF FIBRIN CLOT TO REDUCE FURTHER DAMAGE_1/4 POINTBriefly explain blood vessel repair. _FIBRIN THREADS ATTACHED TO DAMAGED SURFACES OF BLOOD VESSELS GRADUALLY CONTRACT AS PLATELETES PULL IN THEM; AS CLOT RETRACTS PULLS EDGES OF VESSEL CLOSER TOGETHER= DECREASING RISK OF FURTHER INJURY_1/4 POINTDamage to small blood vessels and capillaries frequently occurs. When these vessels are damaged, there are three basic mechanisms that promote hemostasis or the stoppage of bleeding.Following damage, there is an immediate reflex that promotes vasoconstriction, thus diminishing blood loss. Exposed collagen from the damaged site will promote the platelets to adhere.When platelets adhere to the damaged vessel, they undergo degranulation and release cytoplasmic granules, which contain serotonin, a vasoconstrictor, and ADP and Thromboxane A2.The ADP attracts more platelets to the area, and the thromboxane A2 promotes platelet aggregation, degranulation, and vasoconstriction. Thus ADP and thromboxane A2 promote more platelet adhesion and therefore more ADP and thromboxane. The positive feedback promotes the formation of a platelet plug.

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The final hemostatic mechanism is coagulation.Damaged tissue releases factor III, which with the aid of Ca++ will activate factor VII, thus initiating the extrinsic mechanism. Factor XII from active platelets will activate factor XI, thus initiating the intrinsic mechanism.Both active factor VII and active factor XI will promote cascade reactions, eventually activating factor X.Active factor X, along with factor III, factor V, Ca++, and platelet thromboplastic factor (PF3), will activate prothrombin activator.Prothrombin activator converts prothrombin to thrombin.Thrombin converts fibrinogen to fibrin.Fibrin initially forms a loose mesh, but then factor XIII causes the formation of covalent cross links, which convert fibrin to a dense aggregation of fibers. Platelets and red blood cells become caught in this mesh of fiber, thus the formation of a blood clot.

D. Hemostatic Control Mechanisms- page 3611. Small, inappropriate clots dissolve through the process of _FIBRINOLYSIS_1/4 POINT.2. What is the relationship between plasminogen and plasmin? _PLASMINOGEN IS AN

INACTIVE PLASMA ENZYME; IS INCORPAORATED INTO A CLOT. PLASMINOGEN IS ACTIVATED TO PLASMIN BY CERTAIN SUBSTANCES FOUND IN BOTH BODY TISSUES AND BLOOD. PLASMIN IS AN ACTIVE PLASMA ENZYME, WHEN PLASMA IS FORMED IT CAN DISSOLVE CLOTS BY DIGESTING FIBRIN THREADS._ 1/4 POINT

3. Heparin _ANTICOAGULANT; PREVENTS BLOOD CLOTS_1/4 POINT4. Warfarin (Coumadin) _ANTAGONIST TO Vitamin K thus blocking synthesis of 4 clotting

factors; also prevents clotting_1/4 POINTE. Clotting in Blood Vessels- pages 361-362

1. Atherosclerosis _accumulation of fatty substances on arterial walls; result = roughening of endothelial surfaces of blood vessels; now possibility to blood clots forming when blood flows too slowly (allows clotting factors to accumulate)_ 1/4 POINT

2. Pulmonary Embolism _embolism in the lungs; blood clot, bubble of air, fat from broken bones, or piece of debris are causes_1/4 POINT

V. BLOOD GROUPS AND BLOOD TYPESOBJ: Describe the ABO and Rh blood groups. RBC surfaces are marked by genetically determined _glycolipids_ and _glycoproteins_ called _isoantigens_ or _agglutinogens_1/4 POINT.

-distinguishes at least 24 different blood groups i.e. ABO, Rh, etc.A. ABO Blood Group- page 362

1. Based on two glycolipid isoantigens called _A_ and _B_ found on surface of RBCs. 1/4 POINT2. If RBCs 1/4 POINT

- display only antigen A -- blood type _A_- display only antigen B -- blood type _B_- display both antigens A & B -- blood type _AB_- display neither antigen -- blood type _O_

3. Plasma contains isoantibodies or agglutinins to the A or B antigens not found in your bloodanti-A antibody reacts with antigen _A_anti-B antibody reacts with antigen _B_ 1/4 POINT

B. Rh Blood Group- pages 362- 3631. Antigen was discovered in blood of Rhesus monkey2. People with Rh isoantigens on RBC surface are _Rh+_. 1/4 POINT3. People with no Rh isoantigens on RBC surface are _ Rh-_. 1/4 POINT4. Normal plasma contains _no anti-Rh antibodies_.1/4 POINT5. RISK ASSOCIATED WITH Rh- MOTHERS:

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Rh negative mom and Rh+ fetus will have mixing of blood at birthMom's body creates Rh antibodies unless she receives a RhoGam shot soon after first delivery, miscarriage or abortion. In 2nd child, hemolytic disease of the newborn may

develop causing hemolysis of the fetal RBCs

C. Transfusions- pages 363-364

1. Universal Donors and Recipients:a. People with type AB blood called “_UNIVERSAL RECIEPIENT_” since have no antibodies

in plasma. 1/4 POINTb. People with type O blood cell called “_UNIVERSAL DONOR_” since have no antigens on

their cells theoretically can be given to anyone. 1/4 POINT2. Transfusion _transfer of whole blood or blood components (RBCs only or plasma only)

into the bloodstream_1/2 POINT3. Fill in the chart below: 2 POINTS; 1/8 EACH OR 0.16

A B AB O

ANTIGEN A B A and B NEITHER

ANTIBODY B A NEITHER A and B

MAY RECEIVE FROM

A and O B and O ALL O

MAY DONATETO

A and AB B and AB AB ALL

4. FYI (NEED TO KNOW FOR TEST) COMMON DISORDERS:(1) Anemia = Not Enough RBCs

Symptoms:-oxygen-carrying capacity of blood is reduced-fatigue, cold intolerance & palenessTypes of anemia:-iron-deficiency =lack of absorption or loss of iron-pernicious = lack of intrinsic factor for B12 absorption-hemorrhagic = loss of RBCs due to bleeding (ulcer)-hemolytic = defects in cell membranes cause rupture-thalassemia = hereditary deficiency of hemoglobin-aplastic = destruction of bone marrow (radiation/toxins)

(2) Sickle-Cell Anemia (SCA) -Genetic defect in hemoglobin molecule (Hb-S) that changes 2 amino acids at low very O2 levels, RBC is deformed by changes in hemoglobin molecule within the RBC sickle- shaped cells rupture easily = causing anemia & clots-Found among populations in malaria belt: Mediterranean Europe, sub-Saharan Africa & Asia-Person with only one sickle cell gene increased resistance to malaria because RBC membranes leak K+ & lowered levels of K+ kill the parasite infecting the red blood cells

(3) Hemophilia -Inherited deficiency of clotting factors bleeding spontaneously or after minor trauma, subcutaneous & intramuscular hemorrhaging, nosebleeds, blood in urine, articular

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bleeding & pain-Hemophilia A lacks factor VIII (males only) most common-Hemophilia B lacks factor IX (males only)-Hemophilia C (males & females) less severe because alternate clotting activator existsTreatment is transfusions of fresh plasma or concentrates of the missing clotting factor

(4) Leukemia-Acute leukemia uncontrolled production of immature leukocytes crowding out of normal red bone marrow cells by production of immature WBC prevents production of RBC & platelets-Chronic leukemia accumulation of mature WBC in bloodstream because they do not die classified by type of WBC that is predominant---monocytic, lymphocytic.

BLOOD VESSELS NEXT THEN TEST, FOLLOWED BY THE HEART AND FINAL TEST ON CARDIOVASCULAR…

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