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28 Cards in this Set

  • Front
  • Back
A. 5-6L in males, 4-5L in females (average adult volume = 5L)
B. 8% of body weight
C. pH = 7.35-7.45
D. temperature = 100.4 F (body temp = 98.6 F)
E. dense, sticky, viscous, metallic smell, salty taste
F. connective tissue (cells {formed elements: RBC, WBC, platelets} separated by matrix {plasma})
G. 55% = plasma, 45% = formed elements
H. BLOOD ACTIVITIES: provide suitable environment for cellular activities
1. DISTRIBUTION (TRANSPORTATION): oxygen, nutrients, CO2, wastes, hormones
2. REGULATION: body temperature, fluid/solute balance, pH
3. PROTECTION: clotting (HEMOSTASIS), phagocytosis of bacteria, antibodies
II. FORMED ELEMENTS (blood hematocrit):
45% blood volume. WBC, RBC, & platelets produced in bone marrow,
amitotic, short life span
III. ERYTHROCYTES = Red Blood Cells (RBC's)
= 99% of formed elements, just under 45% of whole blood: concentration determines blood thickness

A. biconcave disc creating high ratio of surface area/volume for gas exchange, flexible: able to bend as pass
through small vessels
B. mature cells: anucleate, no organelles. 97% cell occupied by HEMOGLOBIN (HgB) {250 million /RBC} which
transports O2 & CO2
1. HEME = pigment containing iron (4per HgB molecule = 1billion oxygen/RBC)
2. GLOBIN = protein that transports 20% of CO2
3. in lungs: heme + O2 => OXYHEMOGLOBIN (bright red)
4. in tissues: heme no O2 => DEOXYHEMOGLOBIN (dark)
5. in tissues: globin + CO2 => CARBAMINOHEMOGLOBIN
6. smokers:20% heme+CO => permanent non-functional RBC
(hematopoeisis = production of blood) requires folic
acid, Fe and Vit B12

1. In adults, occurs in red bone marrow of: skull, ribs, sternum, ilia, vertebrae, prox. Femur & Humerus
2. RBC's live 120 days: replacement rate: 2 mil. RBC/sec
3. Dead RBC's removed/broken down by spleen, liver
4. Recycled and reused RBC parts returned to red marrow: membrane, Fe, globin
5. ERYTHROPOIETIN: hormone from liver/kidneys released when blood O2 is low: stimulates faster erythropoeisis
Examples of when low blood O2 occur
• high altitude
• increased tissue demands for O2 (exercise)
• smoking: RBC's non-functional due to CO
• ANEMIA: low O2 carrying capacity of blood
• read in text about types of anemias and their causes
IV. BLOOD TYPING AND TRANSFUSIONS (see pages at end of typed outline for “rules” and practice application)
A. if lose > 30% of blood (hypovolemia) -> shock/death
B. many blood typing systems (>14) ABO & Rh are the most important for matching if a transfusion of
whole blood is needed. Other typeable factors include M, N, Duffy, Kell, and Lewis.
C. typing is based on BLOOD FACTORS found on RBC membranes (protein markers = Antigens) and in the
PLASMA (plasma proteins = antibodies = immunoglobulins = gamma globulins)
): item on the RBC membrane that causes a response from plasma antibodies
a. ABO typing system based on two inherited antigens: A and B antigens
If only have A antigens on RBCs = type A blood (40% of population)
If only have B antigens on RBCs = type B blood (11% of population)
If have both A and B antigens on RBCs = type AB blood (4% of population)
If have neither A nor B antigens on RBCs = type O blood (45% of population)

b. Rh typing system based on one inherited antigen: Rh antigen
If the Rh antigen is present on the RBCs = type Rh positive (+) blood
If the Rh antigen is not on the RBCs = type Rh negative (-) blood

plasma protein molecule produced by WBCs in response to a specific Ag.
The Ab will destroy the Ag (cause lysis of cells with the Ag)

* many types found in the blood, but each is very specific, combining only with one type
of antigen

a. Ab of ABO SYSTEM: made just after birth, blood has Ab that react to foreign ABO Ag

ANTI-A reacts with A Ag (will lyse cells with A Ag)
ANTI-B reacts with B Ag (will lyse cells with B Ag)

In type A blood, there are A antigens on the RBCs. B antigens are considered “foreign”. Type A
blood will contain Anti-B antibodies in its plasma to protect it from the introduction of any RBCs
with B antigens on their membranes (type B blood and type AB blood).
: formed ONLY upon exposure to foreign Rh Ag
* one type of antibody: ANTI-Rh

In type Rh + blood, the Rh antigen is present. There is no “foreign” Rh antigen fight off, so there
are no anti-Rh antibodies in Rh+ plasma.

In type Rh- blood, there are no Rh antigens on the RBCs. Rh antigens are considered “foreign”.
Type Rh- blood will develop Anti-Rh antibodies once exposed to the Rh Ag, to fight off any cells
encountered in the future that posess the Rh antigen (Rh + cells).
= determining ABO blood type and/or Rh blood type of a blood sample

1. Blood type is determined by the antigens present on the RBC
2. Remember antibodies destroy antigens of the same name (anti-A Ab destroy cells with A Ag)
3. By taking a drop of blood and adding to it some anti-A Ab, you can determine if A Ag are present.
They will be present if the RBC’s are destroyed (lysis or agglutination occurs). If the drop of blood
does not look any different after the addition of the Ab, then that Ag is not on the RBC!
4. On separate drops of blood you could then test for the presence of B Ag by adding Anti-B Ab and for
Rh Ag by adding anti-Rh Ab.
: increase blood volume and blood pressure, increase number of functional RBCs to increase oxygen-carrying capacity of blood.

*TRANSFUSION RULE: Ab in RECIPIENT’S plasma cannot react with Ag on DONOR’S RBC's. If they do, the result will be a TRANSFUSION REACTION causing lysis of the donated RBC's which may lead to death of the transfusion recipient (ie. Cause a fatal reaction). As long as the recipient will get viable red blood cells from the transfusion, the transfusion will help more than hurt the patient.
1. 85% of population is Rh+ = have Rh Ag on RBC
2. 15% of population is Rh- = no Rh Ag on RBC
a. Rh+, Rh- do not have the anti-Rh antibody in plasma at birth

b. ANTI-Rh Ab will only develop in an Rh- individual if they are exposed (sensitized) to
Rh+ blood cells (and thus the Rh Ag) to destroy the foreign cells. If a sensitized Rh- person is
exposed to Rh+ blood again, will have a TRANSFUSION REACTION
a. Scenario of concern: MOM = Rh- FETUS = Rh+
b. mom exposed to Rh+ blood at birth of Rh+ baby
c. mom develops anti-Rh antibodies in plasma
d. mom = Rh- FETUS2 = Rh+
e. mom's anti-Rh antibodies pass thru placenta lysing fetus' RBC's
f. fetus suffers kidney failure, O2 deficiency, jaundice
g. may be prevented if mom gets RhoGAM shot to prevent anti-Rh formation after first
birth and each consecutive Rh+ birth
LEUKOCYTES (White Blood Cells = WBC's):
large, nucleated cells, no HgB, fewer in # than RBC (less than 1% of
formed elements, less than 1% of whole blood)
A. usually function outside blood taking up residence in loose CNT, lymphatic tissue, other tissues (examples:
osteoclasts, microgila, Langerhan’s cells)
1. DIAPEDESIS: WBC's squeeze out of capillaries

2. CHEMOTAXIS: inflamed tissues emit chemical signal to attract WBC's
granules in cytoplasm, pick up stain, short life span, most are phagocytic
most common WBC (50-70%)
-3-6 lobes in nucleus, small pink granules
-first to damaged tissue, phagocytize bacteria and fungi
not common (2-4%)
-bilobed nucleus, large red granules
-phagocitize histamines from allergic reactions
-destroy parasitic worms
: rarest WBC (<1%)
-bilobed nucleus, large blue granules
-secrete histamine -> vasodilation
-secrete heparin -> anticoagulant
no granules in cytoplasm
: common (25-45%)
-lg. round nucleus, little cytoplasm
-differentiate into Tcells, Bcells and Natural Killer cells
-in immune responses attack viruses and bacteria
-concentrated in lymphatic tissues
not common (3-8%)
-largest WBC -U or C shaped nucleus
-lots of cytoplasm -MACROPHAGES in tissue
-engulf bacteria, dead cells and parts
-work against viruses, parasites, chronic infections
-part of the immune response
b. LEUKOCYTOSIS: increased WBC count as normal response to infection
b. LEUKEMIA: cancer of WBC
c. MONONUCLEOSIS: viral infection causing increase in # of agranulocytes:
lymphocytes and monocytes
. no nuclei, no organelles, smaller than RBC
2. involved in clot formation and HEMOSTASIS
3. 10 day life span
stoppage of bleeding of torn or cut blood vessels (three stages)

A. VASCULAR SPASM = VASOCONSTRICTION: smooth muscle in bv wall contracts

B. PLATELET PLUG FORMATION: platelets stick to bv wall and to each other (positive feedback mechanism)

C. COAGULATION: FORMING THE BLOOD CLOT: FIBRIN (formed from fibrinogen) forms mesh
over tear, catching platelets => CLOT. Clot shrinks, pulling torn edges together. Involves many
clotting factors and VIT K

HEMOPHILIA: deficiency in one or more clotting factors that help coagulation-> bleeding
PLASMA (matrix):
non-living, 55% of blood volume: 90% water, 10% organic/inorganic solutes and gasses

A. PLASMA PROTEINS: most abundant solute (8% of plasma volume), made mostly in liver

1. ALBUMINS (60%): transport molecules, help maintain fluid balance, act as buffers

2. GLOBULINS (36%): alpha and beta types transport fats and vit. ADEK in blood, gamma types make up
ANTIBODIES (gamma globulins)

3. FIBRINOGEN= prothrombin (<4%): blood clotting ** SERUM = plasma – fibrinogen

4. <1% = enzymes, antibacterial proteins, and hormones
Blood Typing Rules: #1-#2
RULE #1: RBC membranes have specific surface proteins (antigens = “Ag”). Ag presence determines blood type.

RULE #2: The plasma will contain Ab (antibodies) to destroy (causing lysis of or agglutination of) any RBCs with Ag other than those on your RBCs. You will not have antibodies in your plasma to destroy your own RBCs!

Possible antibodies in plasma:


Antibody A (anti-A) – destroys cells with A antigens (so found only in plasma of blood without A Ag)
Antibody B (anti-B) – destroys cells with B antigens (so found only in plasma of blood without B Ag)


**Antibody Rh (anti-Rh) – destroys cells with Rh antigens

**this antibody is only produced after an Rh- individual is exposed (sensitized) to cells with Rh antigens
Antibody continued
In type B blood, there are B antigens on the RBCs. A antigens are considered “foreign”. Type B
blood will contain Anti-A antibodies in its plasma to protect it from the introduction of any RBCs
with A antigens on their membranes (type A blood and type AB blood).
In type AB blood, there are both A antigens and B antigens on the RBCs. There are no ABO
antigens that are considered “foreign” so there are no anti-A nor Anti-B antibodies present in the

In type O blood, there are no A antigens nor B Antigens on the RBCs. Both A and B antigens
are considered “foreign”. Type O blood will contain Anti-A and Anti-B antibodies in its plasma
to protect it from the introduction of any RBCs with A antigens or B antigens on their membranes
(type A blood, Type B blood, Type AB blood).
Blood Typing Rules - #3-#4
RULE #3: To determine blood type in the ABO system or the Rh system, find out which Ag are present on the RBC’s. Once you know this, you know the blood type!

By adding Ab (from the lab, not from the blood to be tested) you can determine which Ag are on the RBC’s following the info in rule #2 – if you see agglutination or lysis, then those RBC had the Ag that the Ab destroys!

RULE #4: If more blood is needed through transfusion to raise blood pressure, blood volume, and oxygen carrying capacity, one must determine which types of blood are most compatible with the recipient
*most importantly, the donated RBC’s must “LIVE” (not be agglutinated/lysed) if the recipient is to
live. If the donated RBCs are destroyed, a fatal transfusion reaction will occur!
*Minor (usually not fatal) reactions may occur between the recipient’s RBC Ag’s and the donated
blood’s Ab, but as long as the donated RBCs survive, this transfusion offers greater oxygen transport, blood volume (BP etc.) and is considered an “OK” transfusion.
* the best donors have the same blood type (same Ag on the RBCs and thus the same Ab in the plasma) causing no
transfusion reactions.