Chp
7
Blood
Outline
7-1. Components and functions
of the blood
A- Functions
B- Components
7-2. Hemostasis
7-3. Blood types
7-4. Blood disorders
7-1. Components and functions
of the blood
A- Functions
1. transport: nutrients to cells and remove wastes
2. regulation of temperature, pH, osmotic pressure, glucose, calcium...
3. protection = fight infection (white blood cells)
B- Composition
Hematocrit
- proportion of formed elements in blood.
Enable to detect anemic state. separation of formed elements from
plasma.
http://www.nlm.nih.gov/medlineplus/ency/article/003646.htm
http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/B/Blood.html

a- plasma - yellowish
clear liquid, composed of water, proteins and other solutes.
Water = 90%
Proteins = (all synthesized by the liver)
Albumin = 54%, regulates osmotic pressure
Globulins = 38%, alpha and beta globulins in transport,
gamma globulins in defense (antibodies)
Fibrinogen = 7%, coagulation
Other solutes =
Electrolytes - Na+, K+, Ca++, Mg++
Nutrients - glucose, amino acids, fatty acids, monoglycerides
...
Gases - O2, N2, CO2
Regulatory substance - hormones, enzymes
Vitamins
Wastes
b- Formed elements -
formed from precursor cells or stem cells (hemocytoblast)
located in bone marrow:
formed elements
=>red blood cells or erythrocytes- not true cells
=>white blood cells or leukocytes
=>platelets or thrombocytes- not true
cells
Hematopoiesis or Hemopoiesis
= blood cell formation
Erythropoiesis = red blood cell formation

b1- Erythrocytes (RBC) -
99% of formed elements, bag" filled with hemoglobin (15g/100ml of blood). about 4 to
5 millions RBC per mm3 blood.
Hemoglobin = Globin + Heme : role: carry oxygen

Life Cycle of RBC
- RBCs are formed in red bone marrow
which synthesizes hemoglobin from 4 globin molecules, each
containing 1 heme (each heme
contains 1 iron (Fe).
The erythrocytes have an average life span of 120 days. When RBCs become old
and damaged they are destroyed in spleen and liver by macrophages.
Hemoglobin = globin and heme, globin is recycled; heme is degraded and made of biliverdin
and Fe; biliverdin is green bile pigment which turns into bilirubin (yellow). A small amount passes into the blood and is
eliminated into the urine, giving it its yellow color. In
the intestine, bilirubin is converted into stercobilin (which gives the stools their brown color). The iron is
recycled and transported back to bone marrow.
- Erythropoietin - hormone synthesized by kidney in response to
decreased O2 in blood. This hormone stimulates the bone marrow to produce more red blood
cells
Example: increased altitude => athlete training and blood doping
b2- Leukocytes - formed in
bone marrow, life cycle varies from hours to several years. about 10 000 WBC per mm3 blood

- granular leukocytes
- neutrophils - most numerous 70% role: phagocytosis of bacteria, debris; work
within the blood vessels
- Eosinophils - 3%, destroy parasites
- Basophils - triggers allergic reactions (in the
tissue they become mast cell)
- agranular leukocytes
- lymphocytes - 20%, form antibodies, B-lymph (bone marrow) and T-lymph
(bone => thymus)
- monocytes - phagocytosis of bacteria and debris, in tissue they are called
macrophages (cause pus which is dead
bacteria and dead macrophages)
b3- thrombocytes
= platelets
Derived from breakage of the megakaryocyte
cytoplasm. about 200 000 per mm3 blood. role in hemostasis (to
stop bleeding).
7-2. Hemostasis
Is the ability of the body to stop bleeding.
Trauma to body, such as a cut, exposes connective tissue into the
lumen of the blood vessel

1- Vasospasm (reflex from blood vessel wall), temporary
2- Platelet plug formation - platelets block opening in blood vessel
by sticking to collagen fibers exposed into lumen. They also release serotonin which
maintains vasospasm.
3- Coagulation - damaged tissue releases various factors which
trigger two different chains of reaction, both leading to the formation of fibrin from
fibrinogen
Hemophilia - due to bad coagulation factors, often VIII and IX
Video on coagulation:
-Heparin - Is a thrombin inhibitor. normally secreted in small amount
by basophils and
blood vessel lining.
-Coumadin = Warfarin
- "rat poison", interferes with vitamin K action which is necessary for the
synthesis of several coagulation factors.
http://www.mhhe.com/biosci/esp/2002_general/Esp/folder_structure/tr/m1/s7/trm1s7_3.htm
(animation of the hemostasis process)
http://distance.stcc.edu/AandP/AP/AP2pages/blood/damage.htm
7-3. Blood groups
1- ABO
http://www.biology.arizona.edu/human_bio/problem_sets/blood_types/Intro.html
http://anthro.palomar.edu/blood/ABO_system.htm

Agglutinogens - are antigens that carry a
person's identity. They are embedded in the
cell membrane. In the RBC, the antigens can be
A or B, both or none.
Plasma antibodies which react with the antigens (anti A or anti B). Blood group A with agglutinogen A on RBC has the opposite agglutinin (anti B) in plasma and can never have or make anti-A.
Why can a person A blood type can receive O? Why does this
work?
2- Rh
= Rhesus
Rh+ can
not make anti Rh+
Rh- on RBC able to make anti Rh+ if exposed to Rh+
At birth, there is no Rh agglutinin in
the plasma, but a Rh- person is born with ability to make it.
Examples:
Rh- gets blood with Rh+
1st transfusion - nothing happens = no physical sign but antibodies
anti Rh+ are made
2nd transfusion- Rh+ blood cells are
killed by anti Rh+ => hemolytic reaction
What happens in pregnant women?
-baby Rh- and mother Rh+:
Nothing
-baby Rh+ and mother Rh-: 1st child: no physical sigh but the mother makes antibodies anti Rh+ after the birth of the child. When the second child Rh+ comes along, the baby's blood cells can be destroyed => hemolytic reaction (erythroblastosis fetalis). To save the baby, he will need to have a blood transfusion with Rh- to remove the toxins formed from the hemoglobin degradation and to avoid more hemolysis. To prevent the formation of these agglutinins anti Rh+ by the mother, she is given Rhogam. This drug prevents mother form producing antibodies. Rhogam is nothing else than the antibodies themselves, anti Rh+. They destroy the fetus Rh+ RBC before the mother's immune system has time to react to them. Can only be given early in pregnancy or after the child is born.
http://immuneweb.xxmc.edu.cn/immunology/blood.html
http://anthro.palomar.edu/blood/Rh_system.htm
http://waynesword.palomar.edu/aniblood.htm
Blood types distribution in the world: http://www.warwick.ac.uk/fac/sci/Chemistry/MedChem/MedChemInfo/Blood%20groups/Modern%20Human%20Variation%20Distrib
7-4. Blood disorders
a- Carbon monoxide poisoning: CO, carbon monoxide, has a greater affinity (=liking) to hemoglobin than oxygen. When present, it binds to oxygen and is not easily released. Oxygen, therefore, cannot bind to hemoglobin and is not carried to the tissues where it is needed. The person suffers from headache, flush skin (cherry red), dizziness, nausea, faint and die.
b- Anemia: reduction in oxygen-carrying capacity of the blood à pale skin, fatigue, difficulty breathing..
- iron-deficiency anemia: not enough iron for the hemoglobin molecules, common
- aplastic anemia: the bone marrow does not synthesize enough RBC
- hemorrhagic anemia: due to extreme blood loss
- pernicious anemia: due to deficiency of Vit B12 à immature RBCs
- sickle-cell anemia: genetic disorder where hemoglobin is not normal and the RBCs are shape like a sickleà plug the blood vessels
c- Leukemia: Overproduction of immature and non functional WBCs. Because they take the place of RBCs and platelets in the bone marrow, these are not synthesize
d- Multiple myeloma: abnormal proliferation of myelocytes
e- Mononucleosis: due to a virus, triggering flu-like symptoms, lasting 4-6 weeks.
f- Blood poisoning: due to infection from wound à septicemia. Can be deadly
g- Thrombocytopenia: decreased in platelets, due to viral infection, anemia, leukemia, causes easy bruising and bleeding.
Internet sites of interest:
Tutorials:
www-micro.msb.le.ac.uk/MBChB/bloodmap/Blood.html
www.med.virginia.edu/medicine/clinical/pathology/educ/innes/text/bheme.html
wwwnhc.nhmccd.edu/public/nsci/bio/ap2.html
www.mc.vanderbilt.edu/histo/blood/
Blood groups:
www.umds.ac.uk/elsewhere/tissue/bludgrp.html
Facts about blood donations:
www.lhsc.on/lab/bldbank/blood/page1.htm
Aplastic anemia:
dpalm2.med.uth.tmc/edprog/00000146.htm
Leukemias:
Thalassemia and sickle cell anemia:
cancer.mgh.harvard.edu/medOnc/sickle.htm