g. RBC PRODUCTION-PAGE 355 6 questions @ 1/8 each = 3/4 point

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Name: ___KEY____13.75 points_____________________________________ Period: ____
Chapter 14: THE CARDIOVASCULAR SYSTEM-BLOOD
I. 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 points
OBJ: 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 fragments
Hematocrit: _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 points
Composition:
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 Cells
II. White Blood Cells
A. Granular leucocytes
1. Neutrophils
2. Eosinophils
3. basophils
B. Agranular leucocytes
1. T and B lymphocytes and natural killer cells
2. Monocytes
III. Platelets
1. 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_
OBTAIN A WORKSHEET OF RED BLOOD CELLS THAT SUMMARIZES THEIR FORMATION
c.
d.
e.
f.
g.
h.
Where does hemopoiesis occur before birth? _YOLK SAC OF AN EMBRYO_
Where does it occur in a fetus? _LIVER, SPLEEN, THYMUS, AND LYMPH NODES_
Where does it occur during the last three months before birth? _RED BONE MARROW_
After birth? _RED BONE MARROW_
Red bone marrow is derived from mesenchymal cells called _PLURIPOTENT STEM CELLS
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 points
a. 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 INCH
No _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 blood
Healthy female has about _4.8_ million RBCs/µL of blood
e. RBC LIFE CYCLE-PAGE 354 7 questions @ 1/4 each = 1 ¾ points
Live 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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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
ERYTHROPOIESIS
i. 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 point
a. 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 point
Main function: _COMBAT INFLAMMATION AND INFECTION_
Through process of : _PHAGOCYTOSIS_
Or through: _ANTIBODY PRODUCTION_
NEUTROPHILS AND MACROPHAGES (WHICH DEVELOP FROM MONOCYTES) COMBAT
INFECTION THEORUGH PHAGOCYTOSIS
EOSINOPHILS COMBAT INFLAMMATION IN ALLEGRIC REACTIONS; PHAGOCYTIZE
ANTIGEN-ANTIBODY COMPLEXES, COMBAT PARASITE WORMS
BASOPHILS 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
as well as cardiovascular functions ) IN ALLEGERIC REACTIONS TO INTENSIFY
INFLAMMATORY RESPONSE
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B CELLS EFFECTIVE AGAINST BACTERIA AND OTHER TOXINS
T CELLS AGAINST VIRUSES, FUNGI, AND CANCER CELLS
NATURAL KILLER CELLS ATTACK MICROBES AND TUMOR CELLS
c. WBC LIFE SPAN 2 questions @ 1/8 each = 1/4 point
Life span = _FEW HOURS_ to a _FEW DAYS_
Why??? Can phagocytize only a certain amount of bacteria before interferes with WBC
metabolic activities
Normal blood contains _5000_ to _10,000_ WBCs per µL
LEUKOCYTOSIS = INCREASE IN NUMBER OF WBCs IN NORMAL, PROTECTIVE RESPONSE
TO STRESSES: MICROBE INVADERS, STRENUOUS ACTIVITY, ANESTHESIA, AND SURGERY.
USUALLY INDICATES INFECTION OR INFLAMMATION
DIFFERENTIAL WHITE BLOOD CELL COUNT, COUNTING DIFFERENT WBCs PRESENT SINCE
DIFFERENT ONES COMBAT DIFFERENT THINGS CAN HELP AS A DIAGNOSTIC TOOL
LEUKOPENIAABNORMALLY 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 point
Developed 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 point
Are 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 BLOODSTREAM
Platelets help stop blood loss when blood vessels damaged by forming platelet plug; their
vesicles promote blood clotting
Life span 5-9 days; removed by macrophage in spleen and liver
Structure: _DISK-SHAPED FRAGMENT________________________
Lack a _NUCLEUS_
Normal blood contains _250,000_ to _400,000_ platelets/µL
Complete the ‘Comparison of RBCs, WBCs, and Platelets’ chart on the back of this
page. Table14.2 on page 358 will help.
Table answers = 48 @ 1/16 each = 3 points
4
5
Carry O2 & CO2
(hemoglobin)
Form plug to stop
blood loss;
promote clotting
Combat effects
of histamine;
destroy parasite
worms
Liberate heparin,
histamine, &
serotonin;
intensify
inflammatory
respiration
Phagocytosis
destroy bacteria
Phagocytosis
become
macrophages
Attack invading
virus, cancer &
transplant tissue
cells
Become plasma
cells & secrete
antibodies
Platelets
Eosinophils
Basophils
Neutrophils
Monocytes
T cells
B cells
FUNCTION
Erythrocytes
TYPE OF
CELL
WBCs
20-25% of all
~1000-1500
3-8% of all WBCs
~525
60-70% of all WBC
~4500
WBCs
0.5-1% of all
~75
2-4% of all WBCs
~225
150,000- 400,00
(male) million RBC
4.8 (female) -5.4
NUMBER
PER µL
DRAWING
YES; Large round
& slightly
indented
YES; Kidney or
horseshoe shaped
YES 2-5 LOBES
YES 2 LOBES
YES 2-3 LOBES
NO
NO
NUCLEI?
YES OR NO
NO
NO
NO
NO
NO
NO
NO
YES
HEMOGLOBIN?
YES OR NO
COMPARIOSN OF RBCs, WBCs, AND PLATELETS
Few hours
to days
Few hours
to days
Few hours
to days
Few hours
to days
Few hours
to days
Few hours
to days
5-9 days
120 days
LIFE SPAN
Red bone
marrow;
lymphoid stem
Red bone
marrow;
myeloid stem
Red
Red bone
bone
marrow;
marrow;
myeloid
myeloid stem
stem
Red bone
marrow;
myeloid stem
Red bone
marrow;
myeloid stem
Red bone
marrow;
myeloid stem
Red bone
marrow;
myeloid stem
WHERE
FORMED
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 below
1. 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 below
What is serum? _PLASMA MINUS CLOTTING PROTEINS_1/2 POINT
What is a clot composed of? _A NETWORK OF INSOLUBLE PROTEIN FIBERS CALLED FIBRIN
FILLED WITH TRAPPED FORMED ELEMENTS_1/2 POINT
What 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 POINT
How does hemorrhage occur? _ IF BLOOD TAKES TOO LONG TO CLOT; RESULT =
UNCONTROLLED ENORMOUS LOSS OF BLOOD_1/2 POINT
Refer 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 POINT
1. Clear Retraction and Blood Vessel Repair
What is a clot retraction? _CONSOLIDATON OR TIGHTENING OF FIBRIN CLOT TO REDUCE
FURTHER DAMAGE_1/4 POINT
Briefly 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 POINT
Damage 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.
The final hemostatic mechanism is coagulation.
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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 361
1. 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 POINT
4. Warfarin (Coumadin)  _ANTAGONIST TO Vitamin K thus blocking synthesis of 4 clotting
factors; also prevents clotting_1/4 POINT
E. 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 TYPES
OBJ: 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 POINT
2. 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 blood
anti-A antibody reacts with antigen _A_
anti-B antibody reacts with antigen _B_ 1/4 POINT
B. Rh Blood Group- pages 362- 363
1. Antigen was discovered in blood of Rhesus monkey
2. People with Rh isoantigens on RBC surface are _Rh+_. 1/4 POINT
3. People with no Rh isoantigens on RBC surface are _ Rh-_. 1/4 POINT
4. Normal plasma contains _no anti-Rh antibodies_.1/4 POINT
5. RISK ASSOCIATED WITH Rh- MOTHERS:
Rh negative mom and Rh+ fetus will have mixing of blood at birth
Mom's body creates Rh antibodies unless she receives a RhoGam shot soon after first
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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 POINT
b. People with type O blood cell called “_UNIVERSAL DONOR_” since have no antigens on
their cells theoretically can be given to anyone. 1/4 POINT
2. Transfusion _transfer of whole blood or blood components (RBCs only or plasma only)
into the bloodstream_1/2 POINT
3. 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
A and O
B and O
ALL
O
FROM
MAY DONATE A and AB
B and AB
AB
ALL
TO
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 & paleness
Types 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 sickleshaped 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
bleeding & pain
-Hemophilia A lacks factor VIII (males only) most common
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-Hemophilia B lacks factor IX (males only)
-Hemophilia C (males & females) less severe because alternate clotting activator exists
Treatment 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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