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Chapter 14

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Chapter 14 Powered By Docstoc
					Blood
Dr. Bruce Forciea

This presentation coincides with chapter 17 in the text.

This presentation covers the blood system. We will be learning about blood cells, plasma, hemostasis and blood typing.

Blood
Remember from the tissue section that blood is considered a connective tissue. It contains red blood cells (RBCs), white blood cells (WBCs) and blood fragments called platelets suspended in fluid called plasma. A normal adult has about 5 liters of blood.

If we were to break down blood into its constituent parts we would see…

Cells and Plasma
of blood by volume = cells  55% of blood by volume = plasma
 45%

A measurement of blood cell volume is called the hematocrit (HCT). Sometimes the hematocrit is also called the packed cell volume or PCT. See fig 17-3 p 649

All blood cells come from one precursor cell or stem cell called the hemocytoblast. See fig 17-6 p 652

Blood Cell Origin
cell (hemocytoblast) in bone marrow differentiates into specialized cells.  Colony stimulating factors (growth factors) affect genes in blood cells to guide process of development.
 Stem

The first blood cell we will examine in detail is the red blood cell.

Red blood cells are also known as erythrocytes. They have a unique shape known as a biconcave disk.

A biconcave disk is like a donut where the hole doesn’t go all the way through.

The biconcave disk shape increases the surface area of the cell which allows for a greater area for gas exchange. See fig 17-4 p 650

The primary function of the RBC is to carry oxygen in the bloodstream. The RBC does this because it contains hemoglobin (about 1/3 by volume) which oxygen can attach to. Hemoglobin is what makes the red blood cell red.

RBC
combines with oxygen  Hemoglobin + oxygen = bright red (oxyhemoglobin)  Hemoglobin – oxygen = dull/dark red (deoxyhemoglobin) (can look bluish)
 Hemoglobin

RBCs are relatively simple cells. They do not have many of the structures of other cells.

RBC
There are no nucleus or mitochondria in adult RBCs.

We can measure the number of RBCs in blood. This is called an RBC count.

RBC
blood cell count = number of RBCs in cubic millimeter of blood  4,600,000 – 6,200,000 in males  4,200,000 – 5,400,000 in females  4,500,000 – 5,100,000 in children
 RBC  Red

count increases with exercise and high altitude.

RBCs only live for about 120 days. At the end of their lives they become worn. At one point they wear out enough to fit through capillaries in the liver and spleen where they are broken down and recycled.

When the RBC ―squeezes‖ through the capillaries in the liver and/or spleen it becomes more damaged. After it enters these organs, white blood cells attack the RBCs and break them down (phagocytosis).

The hemoglobin is broken down into heme and 4 globins. The heme is broken down into iron and biliverdin. The biliverdin is converted to bilirubin and secreted in the bile which ends up in the small intestine. The iron combines with transferrin in the bloodstream and is recycled.

The globin gets broken down into amino acids and recycled in the blood plasma— eventually used for synthesis of new proteins. See fig 17-8 p 655

As old RBCs get broken down, new ones must be made to take their places. RBCs are made in the bone marrow. The production of RBCs is called erythropoiesis.

Remember all blood cells come from the hemocytoblast. When blood oxygen levels are low the kidney and liver secrete a hormone called erythropoietin. This hormone is picked up by the bone marrow and facilitates the differentiation of the hemocytoblast into a RBC.

RBC Production
RBC production starts in red marrow.
– Hemocytoblasts erythroblasts – Erythroblasts synthesize hemoglobin
 Nucleus extruded from erythroblast in mature cell to make room for more hemoglobin

– Erythroblasts erythrocytes See fig 17-7 p 653

RBC Production
Some Erythocytes may contain network of tubules (remainder of endoplasmic reticulum). These cells are called reticulocytes. When the endoplasmic reticulum disintegrates the cell becomes a mature RBC.

RBC
life span = 120 days.  Cell may travel through body 75,000 times.  Number of RBCs remain constant via homeostatic mechanism.
 Average

In order to produce RBCs the body needs certain substances.

RBC Production
B12 and Folic Acid important in RBC production.  Vit B12 deficiency usually due to problem in stomach lining – Vit B12 not absorbed due to lack of intrinsic factor (facilitates absorption of B12).  Iron is also needed as small amount is lost daily.
 Vit

RBC Deficiency
Anemia is a reduction in RBCs or hemoglobin.
– Anemia of pregnancy—overall blood volume increases so need more RBCs. – Pernicious anemia—lack of B12.

Check out this information on RBCs at:
http://www.wisc-online.com/objects/index.asp?objID=AP14604

Next we will investigate white blood cells.

Check out table 17-1 p 656 for an overview of all blood cells.

White blood cells are called leukocytes.

WBCs can move around the blood system but do a lot of work outside the blood system.

There are 2 primary categories of WBCs:
1. Granulocytes (granular cytoplasm) 2. Agranulocytes (no granular cytoplasm)

WBCs
Granulocytes
– Big (2 times size of RBC) – 3 kinds
 Neutrophils  Eosinophils  Basophils

WBC
Neutrophil
– Older neutrophils are lobed (polymorphonuclear leukocytes) – Younger called bands (nuclei are C-shaped)

WBC
Neutrophils
– First cell to arrive at site of infection. – Account for majority of leukocytes – Phagocytize bacteria and viruses

WBC
Eosinophils
– 2 lobed nucleus – Granules in cytoplasm – Functions
 Moderate allergic reactions  Defend against parasites
– 1% to 3% of leukocyte population.

WBC
Basophils
– Same size and shape of nuclei as eosinophils – Fewer granules (more irregularly shaped granules) (granules appear blue when stained) – Release histamine – facilitates inflammation – Release heparin – inhibits blood clotting – < 1% population of WBCs

Agranular Leukocytes
The agranular leukocytes do not have granules in the cytoplasm. These are the monocytes and lymphocytes.

Monocytes
blood cells  Nuclei can be spherical, kidney-shaped, oval or lobed.  Monocytes = macrophages (phagocytize bacteria, dead cells and debris)  3% - 9% of WBCs.
 Largest

Lymphocytes
(only slightly larger than erythrocytes)  25% - 30% of WBCs  T-cells
– Directly attack bacteria, viruses, tumor cells, transplanted cells.
 B-cells  Small

– Produce antibodies

WBC Function
WBCs are important in fighting infection
– Phagocytosis of bacteria/virus – Produce antibodies (proteins)— destroy/disable foreign particles.

Diapedesis
WBCs are very mobile and can squeeze between cells and leave circulation. Cellular adhesion molecules guide WBCs to infection. They move via ameboid motion (self-propulsion).

WBCs and Infection
Neutrophils and monocytes are most mobile WBCs.

WBCs and Infection
Bacteria invades tissue  Basophils release histamine  Histamine causes vasodilation—blood vessel leaks  Damaged cells release chemicals that attract WBCs (positive chemotaxis)  WBCs take up bacteria and lyse (kill it) Dead cells form pus

Like RBCs, WBCs can also be counted.

WBC Counts
– 10,000 WBCs per cubic millimeter  If WBC count > 10,000 then have leucocytosis
– Infection – Exercise – Loss of body fluids – Emotional stress
 5,000

WBC Counts
If WBC count < 5,000 = leukopenia
– Typhoid fever – Influenza – Measles, mumps, chicken pox, AIDS, polio – Heavy metal poisoning

WBC counts
Differential
– Breaks out relative percentages of different types of WBCs

Check out these WBCs at:
http://www.wisc-online.com/objects/index.asp?objID=AP14704

The last of the blood cells are not really cells at all but are considered cell fragments.

Platelets
= thrombocytes  Come from megakaryocytes  Platelets more like fragments of cells instead of complete cells.  No nucleus  ½ size of RBC  130,000 – 360,000 platelets per cubic millimeter of blood.
 Platelets

Platelets
Release serotonin—contracts smooth muscles in blood vessels.

Next we will look at blood plasma.

Blood Plasma
straw-colored liquid.  Contains proteins
– Albumin – Globulins – Fibrinogen
 Gases  Clear,

– Carbon dioxide – oxygen

Blood Plasma


Contains nutrients
– – – – Amino acids Simple sugars Nucleotides Lipids



Lipoproteins
– – – – VLDL LDL HDL Chylomicron

Plasma


Contains non-protein nitrogenous substances.
– – – – – Amino acids Urea Uric acid Creatine Creatinine Sodium Potassium Calcium Magnesium Chloride Bicarbonate Phosphate sulfate



Contains electrolytes
– – – – – – – –

The blood can also work to stop bleeding.

Hemostasis is the stoppage of bleeding. There are 3 mechanisms of hemostasis…

Hemostasis
There are 3 mechanisms of hemostasis:
– Blood vessel spasm—vasoconstriction – Platelet plug formation – clotting

Coagulation
Coagulation or clotting is the most effective hemostatic mechanism. Clotting is a result of a sequence of reactions that cause the formation of blood clot (cascade). There are 2 pathways to trigger formation of a clot.
1. Extrinsic 2. Intrinsic

The clotting cascade uses clotting factors. Vit K is important for factors to work.

Clotting Factors
factors are plasma proteins produced in the liver.  Liver needs Vit K to make clotting factors.  Vit K is a fat-soluble vitamin. So need bile to digest it.  In bile obstructions, need to supplement with Vit K before surgery to avoid bleeding.
 Clotting

Coagulation
factors facilitate clotting— procoagulants  Some factors inhibit clotting— anticoagulants Both sets of chemicals kept in balance favoring anticoagulation. When injury occurs procoagulants dominate.
 Some

Coagulation
event = fibrinogen in plasma converted to fibrin.  Fibrinogen is a plasma protein that is normally soluble.  Fibrin is insoluble.
 Major

What Triggers Intrinsic/Extrinsic Clotting?
The 2 pathways leading to clotting are called the extrinsic and intrinsic pathways:  Extrinsic—Release of biochemicals from broken blood vessels/damaged tissue.
 Intrinsic---No

tissue damage, blood contacts damaged endothelial layer of blood vessel walls.

Intrinsic vs. Extrinsic Clotting
clotting—all factors are found in circulating blood.  Extrinsic clotting—Factor III (tissue thromboplastin) is found outside of blood.
 Intrinsic

Extrinsic Clotting
moving outside of vessel activates tissue thromboplastin.  Tissue thromboplastin (factor III) released from damaged tissue.  Factors activated (VIIXV)  Get prothrombin (factor II) converted to thrombin  Thrombin fragments fibrinogen forming fibrin.  Fibrin sticks to exposed surfaces of
 Blood

Extrinsic Clotting
of blood clot causes more clotting to occur—positive feedback.  Clots do not form in bloodstream normally due to prothrombin constantly transported in circulation and presence of antithrombin in vessel walls.  Clotting can then occur in poorly circulating blood or vessels with wall damage.
 Formation

Intrinsic Clotting
of Hageman factor (XII) initiates clotting.  Occurs when blood is exposed to damaged lining of blood vessel.  Factors are activated which activate prothrombin. See fig 17-21 p 665
 Activation

After the Clotting
Blood clot contracts after forming to pull edges of tissue together.  Serum secreted
– Plasma without clotting factors and fibrinogen.
 Clots

eventually absorbed.

– Process called fibrinolysis

Fibrinolysis

Plasminogen activated by thrombin, tissue plasminogen activator, lysosomal enzymes, factor VII

plasminogen

plasmin

Dissolves fibrin

Clotting terms
 Hematoma—clot

leakage  Thrombus—clot forming in vessel  Embolus—thrombus broken loose in bloodstream.  Embolism—clot lodged in blood vessel cutting off circulation.  Infarction—clot forming in vessel to organ (heart, lung, brain).  Atherosclerosis—accumulation of fatty

resulting from blood

Our last topic in this presentation is a discussion about blood typing.

Blood typing is important because if incompatible blood is mixed the result is a clumping of red blood cells called agglutination.

Blood Groups
 Agglutination—reaction

of clumping of RBCs when incompatible blood mixes.
– Happens when antigens (aka agglutinogens) on RBC surface and antibodies (agglutinins) in plasma. – Many types of antigens exist but only a few can cause a serious reaction.

The surface of some red blood cells contain antigens. The plasma contains antibodies.

We can identify the antigens and categorize them according to types A or B.

There is a 3rd antigen that relates to the Rh system of typing called antigen D.

Blood Groups
 ABO

– A person’s RBCs contain 1 of 4 antigen combinations.
    A only (type A) B only (type B) Both A and B (type AB) Neither A nor B (type O)

So type A blood contains type A antigens on the surface and antibody-anti B antibodies in the plasma.

Type B blood contains type B antigens on the RBC surface and antibody anti-A antibodies in the plasma.

Type AB blood has both antigens and no antibodies. Type O blood has neither antigens and both antibodies.

Blood Groups
antibodies produced 2 to 8 months after birth.  If A is absent get antibody anti-A  If B is absent get antibody anti-B So, type A also has antibody anti-B in blood. AND, if type B also have antibody anti-A in blood. AND, if type AB have neither antibody
 Certain

Blood Groups
THUS, a woman and fetus may be of different ABO types and will NOT get agglutination.

Rh Factor
after rhesus monkey.  Several antigens exist most important is antigen D.  If have antigen-D then blood is Rh positive.  If no Rh antigens including D then Rh negative.
 Named

Rh Factors
So, if Rh negative person gets a transfusion from Rh positive person get:
Production of anti-Rh antibodies

Then if get another Rh positive transfusion:
Agglutination

Rh Factors
If Rh-negative woman is pregnant with Rhpositive baby, AND get mixing of blood (at birth) THEN, may get production of anti-Rh antibodies. SO, if woman then gets pregnant with 2nd Rh positive baby –the anti-Rh antibodies cross placenta and cause erythroblastosis fetalis aka hemolytic disease of the newborn.

Play a blood typing game at:
http://nobelprize.org/medicine/educational/landsteiner/index.html

Look at blood typing in action at:
http://www.wisc-online.com/objects/index.asp?objID=AP14804

Check out this blood tutorial:
http://www.getbodysmart.com/ap/circ/circ.htm

The End.


				
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