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.
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
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.
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.
combines with oxygen Hemoglobin + oxygen = bright red (oxyhemoglobin) Hemoglobin – oxygen = dull/dark red (deoxyhemoglobin) (can look bluish)
RBCs are relatively simple cells. They do not have many of the structures of other cells.
There are no nucleus or mitochondria in adult RBCs.
We can measure the number of RBCs in blood. This is called an RBC count.
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
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 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
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.
life span = 120 days. Cell may travel through body 75,000 times. Number of RBCs remain constant via homeostatic mechanism.
In order to produce RBCs the body needs certain substances.
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.
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:
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)
– Big (2 times size of RBC) – 3 kinds
Neutrophils Eosinophils Basophils
– Older neutrophils are lobed (polymorphonuclear leukocytes) – Younger called bands (nuclei are C-shaped)
– First cell to arrive at site of infection. – Account for majority of leukocytes – Phagocytize bacteria and viruses
– 2 lobed nucleus – Granules in cytoplasm – Functions
Moderate allergic reactions Defend against parasites
– 1% to 3% of leukocyte population.
– 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
The agranular leukocytes do not have granules in the cytoplasm. These are the monocytes and lymphocytes.
blood cells Nuclei can be spherical, kidney-shaped, oval or lobed. Monocytes = macrophages (phagocytize bacteria, dead cells and debris) 3% - 9% of WBCs.
(only slightly larger than erythrocytes) 25% - 30% of WBCs T-cells
– Directly attack bacteria, viruses, tumor cells, transplanted cells.
– Produce antibodies
WBCs are important in fighting infection
– Phagocytosis of bacteria/virus – Produce antibodies (proteins)— destroy/disable foreign particles.
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.
– 10,000 WBCs per cubic millimeter If WBC count > 10,000 then have leucocytosis
– Infection – Exercise – Loss of body fluids – Emotional stress
If WBC count < 5,000 = leukopenia
– Typhoid fever – Influenza – Measles, mumps, chicken pox, AIDS, polio – Heavy metal poisoning
– Breaks out relative percentages of different types of WBCs
Check out these WBCs at:
The last of the blood cells are not really cells at all but are considered cell fragments.
= 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.
Release serotonin—contracts smooth muscles in blood vessels.
Next we will look at blood plasma.
straw-colored liquid. Contains proteins
– Albumin – Globulins – Fibrinogen
– Carbon dioxide – oxygen
– – – – Amino acids Simple sugars Nucleotides Lipids
– – – – VLDL LDL HDL Chylomicron
Contains non-protein nitrogenous substances.
– – – – – Amino acids Urea Uric acid Creatine Creatinine Sodium Potassium Calcium Magnesium Chloride Bicarbonate Phosphate sulfate
– – – – – – – –
The blood can also work to stop bleeding.
Hemostasis is the stoppage of bleeding. There are 3 mechanisms of hemostasis…
There are 3 mechanisms of hemostasis:
– Blood vessel spasm—vasoconstriction – Platelet plug formation – clotting
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.
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.
factors facilitate clotting— procoagulants Some factors inhibit clotting— anticoagulants Both sets of chemicals kept in balance favoring anticoagulation. When injury occurs procoagulants dominate.
event = fibrinogen in plasma converted to fibrin. Fibrinogen is a plasma protein that is normally soluble. Fibrin is insoluble.
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.
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.
moving outside of vessel activates tissue thromboplastin. Tissue thromboplastin (factor III) released from damaged tissue. Factors activated (VIIXV) Get prothrombin (factor II) converted to thrombin Thrombin fragments fibrinogen forming fibrin. Fibrin sticks to exposed surfaces of
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.
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
After the Clotting
Blood clot contracts after forming to pull edges of tissue together. Serum secreted
– Plasma without clotting factors and fibrinogen.
– Process called fibrinolysis
Plasminogen activated by thrombin, tissue plasminogen activator, lysosomal enzymes, factor VII
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.
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.
– 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.
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
THUS, a woman and fetus may be of different ABO types and will NOT get agglutination.
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.
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:
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:
Look at blood typing in action at:
Check out this blood tutorial: