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The Physiology of Blood:1/22
• How much blood do we have?
• How do we describe blood and the RBCs found in it?
• How do we form blood and the hemoglobin that
carries oxygen in the RBCs?
• How long do RBCs last in the circulation?
• What happens when RBCs undergo lysis?
• How do we form a hemostasis?
• How do we break up blood clots?
• What are the drugs associated with manipulating the
clotting process?
• 5 point quiz on content of BLOOD LAB at
the beginning of Monday’s lecture!! Read
the lab cerefully prior to Monday.
Quiz: limited to CH 17
Quiz at last 15 minutes at end of monday’s lecture
Please include:
First and Last name
Name Only on side
Watch eraser quality!
Fill dots completely!
Get new scantron if needed
Written questions: ON BACK
Extra Credit: ON BACK
quick return in class monday
Partial List of Functions:
#1: Oxygen/Carbon dioxide#2: Nutrients/Wastes#3: Hormones#4: Protection#5: Transport of HeatCritical Concept: Without hemoglobin inside the erythrocyte,
your blood cannot deliver enough oxygen to keep you alive!
Oxygen has a LOW solubility in water by itself.
What does blood look like: Oxygenated vs. Deoxygenate
HOW MUCH BLOOD DO YOU HAVE? Your body is mostly water
and the blood represents about 8% of your body weight!
(This will be a T.Q.)
If a person weighed 220 lbs, how many liters of blood are there?
If the person lost half their blood how much would you need to
add to replace the lost blood?
Memorize: 1,000 ml H20=1 liter=1 kg= 2.2 pounds
Assume 1kg body wt. is about 1 liter of fluid
How many kg is the person? (220 lbs)(1kg/2.2lb)=100kg
How much blood does the person contain? (100 kg)(0.08)=8 kg
8kg of blood is about the same as 8 liters of blood!
To replace the lost volume you would need 4 liters (half of what
they started with).
Try doing similar calculation for persons with different body
weights on your own or in Supplemental Instruction.
Folks have to do this all the time in an emergency room after
major traumatic accidents.
What does a erythrocyte RBC look like and
what is so special about the shape?
How many erythrocytes do we have in our blood?
About: 5 million/microliter5 billion/ml5 trillion/liter
Typical Size is 2X7.5 micrometers/cell
What happens to the RBC size in hypertonic or hypotonic
environments? When would crenation or lysis occur?
RBCs have donut-like shape to maximize their surface area and the rate
of oxygen and carbon dioxide diffusion into/out of the cell.
Shape? Take a balloon and squeeze two sides towards the center
Are there any RBC Organelles? NO!
• RBCs are Anucleate: they can’t replace proteins if they become
damaged. This limits their life-span to about 120 days and this is a
huge problem!
What are the characteristics used to describe blood and the
erythrocytes that contain the oxygen carrying hemoglobin? For
lect/lab exam be able to interpret MCV, MCH, MCHC and MCD.
RBCs are produced in
the red marrow of
bone in response to
hypoxia and EPO.
RBCs live and deliver
oxygen for about
120 days, but they
get old, damaged
and fragile.
Fragile RBCs are
destroyed by the
spleen and liver.
RBC parts are recycled to make new
With the exception of
heme which leaves
the body in the
urine or feces.
Hypoxia stimulates the formation of the endocrine hormone
erythropoietin (EPO) by the kidney (also liver). EPO promotes
erythropoiesis in the red marrow and ↑↑ O2 carrying capacity.
How Does Erythropoiesis effect PCV and oxygen carrying
capacity of the blood (why is hemoglobin required)?
Hypoxia isAnoxia is notAnemia is-
Polycythemia is not-
What stimulates erythropoiesis?
Why is EPO involved with: Olympic Athletes, High altitude,
Emphysema, Smoking, Cancer treatment!
Why do RBCs provide negative feedback to continue EPO
Excessive erythropoiesis (polycythemia) can be fatal! Why can’t we
live permanently at an altitude of above about 17,000 feet?
What would happen to your circulatory system if the PCV was 60%?
Why is this a potential problem for athletes that abuse EPO?
Why is EPO popular for athletes in the Tour De France?
Erythropoiesis requires making new hemoglobin. Iron is required for
making functional hemoglobin. Iron can only be added to the system
though intake in the diet. Often times people (vegetarians) have
problems related to iron uptake from the gut and develop anemia.
Only 10-35% of Fe++ is absorbed (ferrous iron is type found on hemes in meat)
A meager 2-10% of dietary Fe+++ is absorbed (ferric iron type in most plants)
RBCs last about 120 days. What happens to
RBCs at the end of their functional lifetimes?
Volume produced/day:
• Why does Red Cross get a pint every
56 days?
What are Old RBC/WBC Reserve
Storage Sites: When do they become
clinically significant?
Normal RBC Disposal:
• Extra tiny 2-3 µM passages trap/test
RBCs for viability in Spleen and Liver
• The good cells flex and pass through,
while the old cells rupture (lysis)
Macrophages and remnants create
cellular waste: Biliverdin/bilirubin/bile
Potentially toxic to neonates/adults!
How are the types of anemia clinically categorized?
1) Anemia from Inadequate Erythropoiesis:
-Inability to make Hb-Inability to make RBC-Nutritional causes-Hormonal cause (kidney damage)-Cancer treatment-
2) Hemorrhagic Anemia:
Blood Loss: Acute or Chronic
3) Hemolytic Anemia:
A function of cellular “fragility” Cell Hemolysis
-Sickle Cell Anemia
-Rh Factor and erythroblastosis fetalis
There are Three Sequential Steps that lead to Hemostasis:
Injury to a blood vessel creates a chain reactions that lead to hemostatis.
Does blood need to leave the body when you bleed? (Think Bruises!)
1) Vascular Spasm/Vasoconstriction: Make Vessel Narrower
Injury Pain and synaptic endings on smooth muscle
Also: Epinephrine, Serotonin, Prostaglandins
UltimatelySmooth Muscle Cells Contract and Vessel lumen Narrows
2) Platelet Plug Formation: Platelets adhere to the exposed collagen
and to each other and begin massive degranulation!
Degranulation/Exocytosis releases ADP, Serotonin, Thromboxane
Positive feedback loop is initiated to make other platelets “stickier” to
collagen and each other! Adherent platelets fill hole in vessel!
3) Coagulation or Clotting: Blood Clot Formation
Non-sticky fibrinogensticky fibrinTOUGH FIBRIN POLYMER
“Clotting Cascade” describes the enzyme pathway leading to Polymer.
Prostacyclin and Nitric Oxide
are produced by healthy
endothelial cells and prevent
platelet adhesion to vessel
wall! No Clotting!
Large Clot: “Thrombus”
Coagulation is initiated by chemical signals that originate in the blood
(intrinsic) or tissues (extrinsic). The lack of a factor could be fatal, and
alternately inhibiting any step could save your life!
Heart Attack
The inability to break up clots (fibrinolysis/thrombolysis) is fatal!
Why is thrombolysis important if you experience a heart attack?
How does one balance hemostasis and thrombolysis?
This lets blood
flow to your heart
return after a
blockage by a
Hopefully blood
flow returns
before the infarct
is too large!
How do we manipulate blood clotting clinically?
Plasma: has clotting factors intact
Serum: has clotting factors removed
Factors Preventing Blood Clotting: collagen/tissue factor
Invitro:EDTA vs. calcium, Sodium citrate vs. calcium
Invivo drugs and enzymes:
Coumadin vs. VitaminK
Heparin vs. Thrombin
Aspirin vs. Cyclooxygenase
Genetics: Hemophilia
Factor VIII: 1/5000 males, extremely rare in females
AIDS risk in survivors of hemophilia
Why are hematomas so common in persons taking anticoagulant
medications? Why do they test clotting time so frequently?
Factors Promoting Plasmin and Clot Lysis:
Tissue plasminogen activator and Streptokinase
Anticoagulation therapy and potential for bruising in elderly?
Effects of diet: alcohol, garlic, grapes, cranberries?