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P & A Notes Blood

February 07, 2011

Blood 

The volume of blood varies with size, amount of fat. Avg. male of 154 lbs have about 5.2 quarts.

Blood- about 45% blood cells. The other 55% is clear liquid called plasma. It is in the plasma where both food and wastes are carried.

RBC(erythrocytes)
- Hemoglobin is the red pigment in RBC’s. It is responsible for picking up and carrying oxygen to cells where it is needed. When O2 combines with hemoglobin it becomes bright red. When O2 is given up it becomes darker.
-young RBC have a nucleus.
-Mature RBC reabsorb the nucleus to make more room for hemoglobin.
-There are about 5,100,000 RBC’s/mm3
-Avg. life span of a RBC is about 120 days.
-When RBC are worn out they are broken down by macrophages which are found in the liver and spleen.

Hemoglobin is broken down to heme (iron containing substance) and globin (a protein). Heme is eventually broken down to iron and a pigment called bilirubin. The iron may be taken to blood forming tissue (red bone marrow) to be reused in new hemoglobin. Bilirubin is secreted in bile as a bile pigment.

-About 1/15 of the RBC are removed from circulation each day.
A hemostatic mechanism keeps RBC production and reabsorption in balance.
-The rate of RBC formation seems to be controlled by a hormone erythropoietin.
When there is prolonged O2 deficiency then this hormone is released from the kidneys and some from the liver. This increases RBC production. When tissues receive sufficient O2, then the hormone is no longer released.
-In the embryo RBC are produced in liver, spleen, and yolk sac.
-After birth the RBC are produced in the red bone marrow.
-lack of RBC is called anemia
-vitamins B12 and folic acid are necessary for the production of RBC’s. Actually it is needed to synthesize DNA, which is needed by all cells for growth and reproduction.
-Iron is also needed but not in large amounts because it is reused.
-lack of iron results in hypochromic anemia --> small pale RBC
-women need to take iron supplement due to menstruation.

White Blood Cells: Leukocytes
Function: Defend against microbes. WBC’s do much of their work outside the circulatory system, but they use it for transportation. WBC’s are grouped into 2 groups.
Granulocytes- cells with granular cytoplasm
Agranulocytes- cells lacking granular cytoplasm

Granulocytes are: 1.)Neutrophils 2.)Eosinophils 3.) Basophils
Agranulocytes are: 1.) monocytes 2.)lymphocytes

-There are from 5000-10000 WBCs/mm3 of blood.
-What would a rise in this count indicate?
-A rise is called leukocytosis and occurs during severe infections. (appendicitis)
-If it drops below 5000 then it is called lucopenia. May be caused by typhoid fever, influenza, measles, mumps, chicken pox, poliomyelitis.
Why would a differential WBC count be useful?

The various leukocytes react different to different types on infections. (Neutrophils increase with bacterial infections. Eosinophils increase during parasitic infections).

Functions of WBC:
(see chart 12:1 pg 329)

-Not all WBC can phagocytize. Some produce antibodies that react with microbes to destroy and disable them.
That is why anteaters don’t get sick!
Leukemia- Uncontrolled production of leukocytes that don’t mature. these leukemic cells soon crowd out the normal cells and lower the victims resistance to infection.

Blood Platelets/ Thrombocytes
A platelet isn’t a complete cell. It is a fragment. In normal blood the platelet count will vary from 130,000 to 360,000/mm3 of blood.
Function- help close breaks in damaged blood vessels. Help in the formation of blood clots. WBC, RBC and platelets make up the solid portion of blood called hemocrit. Hemocrit makes up about 45% of the blood. the other 55% is the liquid portion called plasma. What are the contents of plasma?
-about 92% H2O..... (pg483)

Functions: transport nutrients, gas, vitamins, regulate fluid and electrolyte balance, maintaining P.H., moving hormones.....cell waste....
Most abundant dissolved substance is plasma proteins. Are not used as an energy source. they remain in the blood and interstitial fluid.

Albumins, a plasma protein that makes up over 60% of all the plasma proteins in the blood. Plays major role in maintenance of osmotic pressure of the blood. (H2O goes from low --> high O.P.)
-Helps to control blood volume, which is directly related to blood pressure.

Globulins- About 36% of the plasma proteins. alpha and beta globulins are both produced in the liver.
Function: transport lipids and fat soluble vitamins and many others.
Gamma globulins are produced by the lymphatic tissues and function as antibodies.

Fibrinogen- largest plasma protein. Produced by liver. Plays vital role in formation of a blood clot.

Other substances in plasma:
nutrients (amino acids, simple sugars, various lipids), O2 and CO2 and dissolved nitrogen. Urea and uric acid, which are wastes of protein and nucleic acid catabolism. --> Removed by kidney and excrete in the urine.
What would a rise in nitrogenous waste suggest?
(Kidney disorder or excessive protein catabolism or infection.)
Many electrolytes are also found in the plasma--important in maintaining osmotic pressure and P.H.

Hemostasis (stoppage of bleeding)
following an injury to a blood vessel, several things happen to prevent excessive blood loss. These include blood vessel spasm, platelet plug formation and blood clot formation.
Is most effective in small vessel such as arterioles, capillaries, and venules.
-When an arteriole or venule is cut the smooth muscles in its walls are stimulated to contract. This blood vessel spasm results from stimulation from the vessel wall and from pain receptors in the injured tissue, however this spasm will last only a few minutes.
Platelets will stick to the ends of the injured vessel and to the collagen in the loose connective tissue that lies under the simple squamous epithelium lining (endothelial) of the blood vessel. Platelets will release serotonin causing a prolonged blood vessel spasm.
When platelets contact collagen, their shapes change. Spiny processes stick out from their membranes and they stick to each other and to the collagen, forming a platelet plug.
When blood comes in contact with damaged blood vessels or tissue outside the blood vessel it releases substance called tissue thromboplastin. This initiates the production of prothrombin (plasma protein) to be converted to thrombin (calcium must be present). Thrombin acts as an enzyme which causes fibrinogen to be converted to fibrin threads. This reaction also needs calcium ions present.
The fibrin threads stick to each other and to the damaged vessel forming a meshwork...blood cells and platelets get caught in this mesh and form a clot.

When a clot forms in a vessel abnormally it is called a thrombus.
(may happen with atherosclerosis)

If the clot moves, or a portion breaks off and is carried away--then it is called an embolus.
The embolus will eventually get lodged in a narrow vessel and interfere with blood flow.
If lodged in the coronary artery...-->
heart attack
If lodged in one of the branches of the carotid artery...--> stroke

* What prevents an abnormal clot?

*Tissue thromboplastin produced from the same damaged cells initiates this chain reaction.... What prevents the formation of a massive clot?

1. The simple squamous epithelium
( endothelium) of the blood vessels carries a negative charge and repels the platelets.
2. The endothelial lining of the blood vessels produce antithrombin.
3. The blood vessel lining produces a substance called prostacyclin, which inhibits the adherence of platelets to its surface.
4. Clot forming fibrin threads absorb thrombin preventing the spread of the clotting action.
5. A plasma protein called antithrombin, which is normally present in the plasma, binds to thrombin and blocks its action.
6. Basophils and mast cells secrete heparin. Heparin interferes with formation of prothrombin activator.
7. Moving blood carries away excess thrombin, diluting it un the blood preventing further clotting.

- What causes the change in the platelets, causing them to stick to each other during plug formation?

- Prothrombin is a plasma protein found in the blood. Normal calcium levels in the blood is 8.5 - 10.5mg per 100mL of blood. In your text, it says that prothrombin is converted to thrombin in the presence of calcium. Why does his normally happen only when there is tissue damage?
- How does a blood vessel spasm control bleeding?

Blood typing-
Doctors once used direct transfusion from one person to another.
Sometimes it helped the person.... Sometimes the problems got more serious or they even died.
-When you mix two different blood types and the RBC clump... it is call agglutination.
-RBC membrane has antigens (agglutinogens).
-Plasma has protein antibodies (agglutinins).
-when the wrong kinds of antigens and antibodies mix then agglutination results.

-Scientists began to type blood. There are many types of antigens but only a few cause serious transfusion problems. These are of the A,B,O groups and of the Rh group.
-Each person has RBC that contain one of a combination of antigens: only A, only B, both A and B, or neither A or B (called O)
-If a person is lacking A antigen in their RBC then an agglutinin / antibody called anti-A is present in the plasma. If B is absent then anti-B is present.
-If you mix A with anti-A it would cause agglutination.
Blood matching:
O

A B

AB

-O blood has anti-A and anti-B.
-Normally they match type for type. If the same type isn’t available then they transfuse slowly so the donor’s blood will dilute with the recipient’s and lower the chance of agglutination.

-Blood types are inherited factors
-Rh group got its name from the rhesus monkey where it was first observed.
-If any of the Rh factors are present in the membrane of the RBC, then it is Rh positive. If they are absent then it is Rh negative.
-If an Rh negative receives Rh positive blood, the recipients antibody producing cells will be stimulated to begin producing anti - Rh agglutinin.
* 1st time there is no serious effects from it
* With next transfusion anti - Rh antibodies are already present and blood will agglutinate.
* If an Rh - woman is pregnant with an Rh positive fetus. 1st pregnancy, during birth, the placental membrane that separated maternal blood from fetal blood will be broken, stimulating the mother to produce anti-Rh agglutinins. The risk is is the second pregnancy where there could be mixing again causing agglutination. Agglutination in the fetus causes the disease erythroblastosis fetalis

-Prevention: Treat mom with a blood serum from an Rh negative person with anti-Rh antibodies. This inactivates any Rh positive cells that enter the mothers blood and keeps her from forming anti-Rh.

Result of agglutination:

-Agglutinated cells are destroyed by phagocytic cells. Hemoglobin is broken to heme and globin ----> eventually to bilirubin (yellow pigment)

-Free hemoglobin may pass into kidneys and cause kidney failure.

-Infants born with erythroblastosis fetalis usually have jaundice, severely anemic, kidney failure, permanent brain damage.

 

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