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Transcript
Unit 9
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Blood is the only fluid tissue in the body
Although it appears to be thick and uniform,
it is actually composed of solid and liquid
components
Blood cells = formed elements
Non-living fluid = plasma
Red blood cells = erythrocytes
White blood cells = leukocytes
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Erythrocytes make up ~45% of the volume of a
blood sample  this percentage is called the
hematocrit
Leukocytes make up less than 1% = buffy coat
Plasma makes up the remaining ~55%
Oxygenated blood looks bright red
Deoxygenated blood looks dull red
pH between 7.35 and 7.45
~8% of body weight, 5-6 liters
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90% water
Contains over 100 different substances,
including nutrients, metal ions, respiratory gases,
hormones, proteins, and other cell metabolism
products  composition varies continuously
Most abundant solutes are plasma proteins 
mainly made in liver, serve a variety of functions
Albumin = helps maintain osmotic pressure of
blood by keeping water in the bloodstream
Clotting proteins stem blood loss
Antibodies protect body from pathogens
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Plasma composition varies continuously, but
is kept relatively constant through
homeostatic mechanisms
Acidosis = blood is too acidic
Alkalosis = blood is too basic
Liver, kidneys, respiratory organs, etc. work
to keep plasma composition stable
Plasma helps transport various substances
and distribute body heat evenly throughout
the body
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Red blood cells (RBCs) – carry oxygen to all cells
in the body
Don’t have a nucleus, very few organelles
Mature RBCs are just sacs of hemoglobin
molecules
Hemoglobin (Hb) is a protein that contains iron
and helps transport oxygen and carbon dioxide
RBCs don’t have mitochondria  make ATP using
anaerobic respiration, so they don’t use the
oxygen they are transporting
Shaped like biconcave disks  doughnuts
Outnumber white blood cells 1000 to 1
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1 RBC can carry 1 billion molecules of oxygen
Increase in number of RBCs is called polycythemia
A decrease in the oxygen carrying ability of the blood
is called anemia
Anemia can be caused by a decrease in the number of
RBCs or by a lower hemoglobin content in the RBCs
Sickle-cell anemia – abnormal hemoglobin causes RBCs
to collapse and lose flexibility  “sickle shape”
These cells rupture easily and clog up small vessels
Causes inhibited oxygen delivery, extreme pain, and
advantage for surviving malaria parasite
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White blood cells – WBCs
The only “complete” cells in the blood  contain
nuclei and organelles
Defense against disease
Able to slip in and out of blood vessels (diapedesis)
Positive chemotaxis – WBCs can detect tissue
damage, infection, etc. by “sniffing out” the chemicals
these events release
Leukocytosis – WBC count above average, indicates
infection
Leukopenia – low WBC count, usually caused by drugs
Leukemia – “white blood,” bone marrow becomes
cancerous and starts making huge numbers of WBCs
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Two major groups:
◦ Granulocytes = contain granules, have lobed nuclei
 Neutrophils = phagocytes, short-term or acute infections
 Eosinophils = kill parasitic worms, increase for allergies
 Basophils = contain histamine, cause inflammation and
attract other WBCs
◦ Agranulocytes = lack visible granules, more spherical
nuclei
 Lymphocytes = B lymphocytes make antibodies, T
lymphocytes fight tumors and viruses (and reject grafts)
and activate B lymphocytes
 Monocytes = long-term “clean-up team,” chronic
infections
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Not exactly cells  more like fragments of
cells called megakaryocytes
Needed for clotting process when blood
vessels rupture or are broken
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Occurs in red bone marrow
All blood cells start out as a hemocytoblast, a
common type of stem cell
Becomes either lymphoid or myeloid stem cell
Lymphoid stem cell becomes lymphocyte
Myeloid stem cell can become any other kind
of blood cell
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RBCs are anucleate = they are unable to
synthesize proteins, grow, or divide  fall
apart in 100 to 120 days
Lost cells are constantly replaced by the
division of hemocytoblasts in red bone marrow
Erythropoietin = hormone that controls rate of
RBC production, made by liver and kidneys
Colony stimulating factors (CSFs) and
interleukins = stimulate WBC production
Thrombopoietin = stimulates platelet
formation
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Hemostasis = stoppage of blood flow
When a blood vessel wall breaks, a series of
reactions is set in motion
1. Platelet plug forms – Platelets (which are
normally repelled by healthy endothelium) stick
to the now-exposed “sticky” collagen fibers.
They release chemicals that attract more platelets
until a platelet plug (white thrombus) is formed.
2. Vascular spasms occur – Platelet plug starts to
release serotonin, which causes blood vessel to
spasm. This narrows the blood vessel, which
reduces blood flow.
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3. Coagulation events occur –
◦ A. Injured tissues release thromboplastin, which plays
important role in clotting.
◦ B. PF3 = phospholipid that coats surfaces of platelets. It
interacts with thromboplastin, other clotting factors, and
calcium ions to make an activator that triggers the clotting
cascade.
◦ C. The prothrombin activator turns prothrombin to
thrombin.
◦ D. Thrombin joins fibrinogen proteins into long, hairlike
molecules called fibrin. The fibrin forms a “net” that traps
RBCs and forms the clot. After an hour, the clot will start
to retract, which squeezes out serum (plasma minus
clotting proteins) and pulls the broken edges of the blood
vessel closer together.
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Entire process normally takes 3-6 minutes
Applying sterile gauze can speed up the
process because the gauze provides a rough
surface for platelets to stick to.
Applying pressure will rupture nearby cells,
which increases the release of
thromboplastin.
http://www.youtube.com/watch?v=9QVTHD
M90io&feature=related
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Two major problems: too much clotting or
not enough
Too much clotting:
◦ Thrombus – a clot that develops and persists in an
unbroken blood vessel
◦ Embolus – a thrombus that breaks away from the
vessel and floats freely in the blood stream
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Not enough clotting:
◦ Thrombocytopenia – not enough platelets
◦ Hemophilia – hereditary disorder resulting in lack of
any of the factors needed for clotting
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Plasma membranes of RBCs contain antigens.
Antigens = substance the body can recognize as
foreign  stimulates release of antibodies to
attack them
Antibodies recognize “native” antigens and
“foreign” antigens
Antibodies will bind to foreign antigens and
cause RBCs to clump together = agglutination
This can cause blocked vessels, kidney blockage
and failure, fever, chills, nausea, vomiting, etc.
Over 30 RBC antigens, but the ABO and Rh
antigens cause the most severe reactions
Blood group
RBC antigens Plasma
antibodies
Can receive
from
Can donate
to
AB
A, B
None
A, B, AB, O
(universal
recipient)
AB
B
B
Anti-A
B, O
B, AB
A
A
Anti-B
A, O
A, AB
O
None
Anti-A,
Anti-B
O
A, B, AB, O
(universal
donor)
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Rh factor – originally discovered in Rhesus
monkeys
Rh+ = RBCs carry Rh antigen
Rh- = RBCs do not carry Rh antigen
Anti-Rh antibodies are only formed after Rh
antigens are detected in a Rh- person.
If an Rh- woman is pregnant with a Rh+
baby, she must take RhoGAM right after
delivery or she will develop anti-Rh+
antibodies that will attack her next
pregnancy.