85 terms

Ch 14 Blood and Blood Cells

percentage of cells in blood volume (approximately 45%)
1. Red blood cells
2. White blood cells
3. Platelets
Types of Cells
Bone marrow
originate as hemocytoblasts (stem cells)
Red blood cells or __________(RBC)
a. Increases surface area for gas transport
b. Places the cell membrane closer to hemoglobin (oxygen carrying protein)
c. Allows the cell to squeeze thru narrow capillaries
Bioconcave of RBCs shape helps by:
Red Blood Cells
1. Small= 7.5um in diameter
2. Biconcave shape Fig. 14.4
a. Increases surface area for gas transport
b. Places the cell membrane closer to hemoglobin (oxygen carrying protein)
c. Allows the cell to squeeze thru narrow capillaries
3. Mature RBCs lack nuclei- cannot synthesize mRNA & proteins
4. Lack mitochondria- produce ATP only by glycolysis so they don't utilize any of the oxygen that they carry
a. With age become damaged when passing thru capillaries especially in active muscles
b. Damaged RBCs rupture when passing thru liver & spleen
c. Macrophages in these organs phagocytize the cellular debris
d. Hemoglobin released by dying cells breaks down into 4 globin chains each surrounding a heme group Fig. 14.8
i. Heme further breaks down into iron plus a greenish pigment biliverdin
ii. Some iron can combine with transferrin (protein) & be carried back to red marrow for recycling
iii. About 80% of iron is stored in the liver as an iron-protein complex called ferritin
iv. Biliverdin is converted to bilirubin & both are secreted in bile salts
When RBCs wear out or become damaged, they are removed by the liver and spleen:
b. Typical range male= 4.6-6.2 million female= 4.5-5.1 million
c. Used to diagnose & evaluate certain diseases
RBC counts
RBC Production
a. Initially occurs in yolk sac, liver & spleen
b. After birth occurs exclusively in red marrow of spongy bone
c. Within red marrow hemocytoblasts give rise to erythroblasts
d. Erythroblast synthesize hemoglobin
e. Nuclei shrink & are extruded from the cell by exocytosis & cell becomes a reticulocyte
f. Reticulocytes contain a remnant of endoplasmic reticulum & this is the stage that exits the bone marrow
g. When the reticulum degenerates the cell becomes a mature erythrocyte
h. Average lifespan of an erythrocyte is 120 days (travels thru the body 75,000 times)
i. Negative feedback mechanism controls RBC production
i. In response to prolonged oxygen deficiency the hormone erythropoietin is released primarily by the kidneys & to a lesser extent by the liver
ii. Travels via the blood to red marrow & stimulates erythrocyte production
iii. After a few days the number of circulating erythrocytes increases
iv. Oxygen delivery increases & erythropoietin release decreases
Negative Feedback Mechanism
i. In response to prolonged oxygen deficiency the hormone erythropoietin is released primarily by the kidneys & to a lesser extent by the liver
ii. Travels via the blood to red marrow & stimulates erythrocyte production
iii. After a few days the number of circulating erythrocytes increases
iv. Oxygen delivery increases & erythropoietin release decreases
___________mechanism controls RBC production
i. Increase in altitude- drop in atmospheric pressure
ii. Strenuous exercise
iii. Blood loss
iv. Chronic lung disease
Decrease in oxygen delivery caused by________(4)
i. Vitamin B12 & folic acid- required for DNA synthesis in rapidly dividing cells (deficiency due to lack of intrinsic factor that is produced by cells in the stomach & is needed for vit B12 absorption)
ii. Iron is required for hemoglobin synthesis- much of the iron is recycled but some is lost each day & must be replaced (iron absorption is slow & only a small fraction of ingested iron is absorbed, the rate of absorption depends on the level within tissues)
iii. Vitamin C increases absorption of iron in the digestive tract
Dietary Factors in RBC production:
a. Reduces oxygen carrying capacity of blood
b. Results in fatigue & pale skin color
c. Can occur during pregnancy due to increase in fluid volume
Anemia- lack of RBCs or hemoglobin causes: (3)
1. Protect against disease and infection Fig. 14.15
2. Types- distinguished by size, nature of the cytoplasm, shape of the nucleus & staining characteristics
White blood cells (WBC) (leukocytes) purpose (2)
Neutrophils- (polymorphonuclear leukocytes) first to arrive at a site of infection & phagocytize bacteria, fungi & some viruses Fig. 14.9
iv. Eosinophils- moderate allergic reactions & defend against parasitic worm infestations Fig. 14.10
v. Basophils- migrate to damaged tissue & release histamine (promotes inflammation) & heparin (inhibits clotting which increases blood flow to injured tissues) Fig. 14.11
b. Agranulocytes
i. Monocytes- largest blood cells, leave the bloodstream & become macrophages (phagocytize bacteria, dead cells & cellular debris), contain numerous lysosomes with digestive enzymes Fig. 14.12
ii. Lymphocytes Fig. 14-13
iia. T cells- attack microorganisms, tumor cells & transplanted cells
iib. B cells- produce antibodies which are proteins that attack foreign cells or proteins
Types of Granulocytes (WBCs)
12 hrs
Lifespan of WBC
2x that of RBCs
Size or WBC
can squeeze thru openings in capillaries and leave the bloodstream (diapedesis) Fig. 14.14
4. Cell adhesion molecules help to guide leukocytes to the site of injury
5. Damaged cells release chemicals that attract them (positive chemotaxis)
a. Infection
b. Vigorous exercise
c. Emotional disturbances
d. Great loss of body fluids
Leukocyte increase (WBC) greater that 10,000 caused by:
a. Disease- typhoid fever, AIDS, influenza, measles, mumps, chicken pox, poliomyelitis
b. Anemia
c. Poisoning- lead, arsenic, mercury
WBC decrease (less that 5,000) caused by:
Differential WBC count (DIFF)
__________breaks down percentages of each type of leukocyte
Increased neutrophils
- bacterial infections
Increased eosinophils
certain parasitic infections -(tapeworm & hookworm) & allergic reactions
Decrease in helper T cells
- HIV infection
Increased lymphocytes
- hairy cell leukemia, whooping cough, mononucleosis
Increased monocytes
typhoid fever, malaria, tuberculosis
E. Platelets (thrombocytes)
1. Megakaryoblasts become megakaryocytes that are stimulated by thrombopoeitin to break apart into fragments of cells
2. Become platelets as they pass thru the blood vessels in the lungs
3. Capable of ameboid movement
4. Live for about 10 days
5. Count- 130,000-360,000 per cubic milliliter
6. Help to repair damaged blood vessels by sticking to broken surfaces
7. Release serotonin which contracts smooth muscle in vessel walls reducing blood flow
straw colored liquid, 92% water, mixture of organic & inorganic molecules
Functions of Plasma
a. Transports gases
b. Transports nutrients & vitamins
c. Regulates fluid & electrolyte balance
d. Maintains pH
Plasma proteins
non-protein nitrogenous substances
Albumins in plasma
i. Synthesized in liver
ii. Abundant- 60% of plasma proteins
iii. Major determinant of osmotic pressure- holds water in capillaries despite blood pressure causing loss of water by filtration & therefore regulates fluid volume
iv. Binds & transports free fatty acids, bilirubin, hormones & certain drugs
Globulins in plasma
i. Alpha & beta- synthesized in liver, transport lipids & fat soluble vitamins
ii. Gamma- type of antibody synthesized in lymphatic tissue
c. Fibrinogen- synthesized in liver & involved in blood coagulation
Gases in plasma
oxygen, carbon dioxide & nitrogen
Nutrients in plasma
a. Amino acids
b. Simple sugars
c. Lipids Table 14.8
Lipids in Plasma
i. Carried by lipoprotein complexes
ii. Include apoprotein, cholesterol & phospholipids on the surface & a triglyceride core
iii. Receptors on the surface of cells can bind to the apoproteins & endocytose the complex
iv. Lipoprotein complexes
iva. Chylomicron- high concentration of triglycerides, transports dietary fats to adipose & muscle cells
ivb. Very low density lipoproteins (VLDL)- high concentration of triglycerides, transports triglycerides from liver to adipose tissue
ivc. Low density lipoproteins (LDL)- high concentration of cholesterol (formed from VLDL that have given up their triglycerides), delivers cholesterol to cells
ivd. High density lipoproteins (HDL)- high concentration of proteins, transports chylomicron remnants (given up their triglycerides) to the liver
v. Liver cells dispose of cholesterol by secreting it into bile (gall bladder) which is released into the intestine as bile salts
vi. Cholesterol & bile salts are then reabsorbed by the intestine & transported to the liver completing the cycle
Non protein nitrogenous substances in plasma
a. Amino acids- protein degradation
b. Urea- product of protein catabolism BUN- blood urea nitrogen
i. Half the non protein nitrogenous substances is urea
ii. Excreted by the kidneys
iii. Elevated BUN could be kidney disorder, excess protein catabolism, or infection
c. Uric acid- product of nucleic acid catabolism
d. Creatinine- product of creatine (stores high energy phosphate bonds in muscle & brain tissue) catabolism
stoppage of bleeding
Blood vessel spasm
1. Cutting or breaking vessel stimulates smooth muscle to contract
2. Stimulation of pain receptors also stimulates contraction of smooth muscle
3. Lasts about thirty minutes by this time a platelet plug has formed
4. Platelets release serotonin which causes vessels to contract
1. Platelets stick to exposed ends of blood vessels especially collagen in connective tissue
2. After contact with collagen, platelets change shape & spiny processes protrude from cell
3. Platelets also stick to each other forming the platelet plug
Platelet plug formation
Blood coagulation- formation of a blood clot
1. Extrinsic clotting mechanism- release of biochemicals from broken blood vessels or damaged tissue
a. Release of clotting factors from disrupted cell membranes triggers the clotting cascade culminating in the production of thrombin from prothrombin
b. Thrombin catalyzes the formation of fibrin from fibrinogen (prothrombin time)
c. Fibrin entraps blood cells & platelets forming a blood clot
d. The production of thrombin is proportional to the extent of tissue damage & is an example of positive feedback
e. Normal blood flow prevents the formation of clots by removing thrombin from the area
f. Clotting occurs in an area where blood is standing still or slow moving & ceases when a clot encounters circulating blood
2. Intrinsic clotting mechanism- blood contacts foreign surfaces in absence of tissue damage
a. All of the components necessary for intrinsic cascade are in blood itself
b. Collagen in connective tissue instead of endothelial cells lining blood vessels would constitute a foreign surface
Fate of blood clot (thrombus)
1. Blood clot shrinks
2. Platelets within the clot release platelet derived growth factor (PDGF) which stimulates smooth muscle cells & fibroblasts to repair damaged blood vessels
3. Plasmin is produced which digests fibrin
4. A blood clot that dislodges & is carried by the bloodstream is called an embolus
5. If an embolus ends up in a small vessels & blocks blood flow it is called an embolism
6. Infarction- death of cells supplied by a vessel that is blocked by a thrombus or embolus
7. Abnormal clot formation Fig. 14.20
a. Atherosclerosis- clot formation in an artery with accumulations of fatty deposits
b. Clotting may occur in blood that is flowing too slowly (usually occurs in veins)
Prevention of blood coagulation
1. Smooth endothelial lining of healthy blood vessels inhibits clot formation
2. Endothelial cells produce prostaglandins that inhibits the adherence of platelets to surface of blood vessels
3. Plasma alpha globulin called antithrombin binds to thrombin & inactivates it
4. Basophils & mast cell in surrounding connective tissue secrete the anticoagulant heparin
5. Heparin secreting cells are abundant in liver & lungs where capillaries trap small blood clots that commonly form in the slow moving blood of veins
a. Antigen A
b. Antigen B
c. Antibody anti-A
d. Antibody anti-B
ABO blood groups
a. A- has antigen A & anti-B
b. B- has antigen B & anti-A
c. AB- has antigen A & B, has no anti-A or anti-B (universal recipient)
d. O- has no antigen A or B, has anti-A & anti-B (universal donor)
Blood Types
1. Several Rh antigens (most important is D)
2. If RBCs have any of the Rh antigens on their surface they are Rh-positive
3. Those RBCs that lack Rh antigens are Rh-negative
4. Rh antibodies do not form spontaneously in Rh-negative individuals but only in response to transfusion with Rh-positive blood
5. First transfusion is usually not a problem but a second transfusion with Rh-positive blood will cause agglutination in an Rh-negative person because they have become sensitized to the antigen (produces large quantities of antibody after the second exposure)
Rh blood group
a. Rh-negative woman + Rh-positive man conceive an Rh-positive child
b. Some of the Rh-positive blood crosses the placenta during the first pregnancy at birth, miscarriage, termination of pregnancy or during amniocentesis & enters the maternal bloodstream producing Rh-positive antibodies in the mother (sensitization)
c. During the second pregnancy with an Rh-positive child, the mothers anti-Rh antibodies can cross the placenta & attack the fetal RBCs (erythroblastosis fetalis)
d. Prevented by giving the mother RHoGAM, a drug that binds maternal RH antibodies within 72 hours of birth, miscarriage, termination of pregnancy or amniocentesis
Rh blood group problems in pregnancy
Hypoxia (cyanosis)
1. Prolonged oxygen deficiency
2. Extreme cold (constricts superficial blood vessels)
3. Skin & mucous membranes appear blue due to high levels of deoxyhemoglobin
B. Sickle cell
1. Single DNA base change
2. Results in abnormal hemoglobin that crystallizes in oxygen deficient environments
3. Bends cell into sickle shape
4. Blocks circulation in small vessels
5. Causes excruciating joint pain, organ damage & increased susceptibility to infection (spleen works overtime to recycle abnormal RBCs)
6. Treatment- bone marrow transplant or hydoxyurea (activates alternate hemoglobin gene)
1. Small intestine absorbs too much iron
2. Accumulates in pancreas, heart, liver, endocrine glands & turns skin bronze
3. Increased risk of infection (bacteria thrive in iron-rich environment)
4. Treatment- periodic removal of blood
1. Erythrocytes are more sensitive to erythropoietin
2. Individuals produce 25% more RBCs
3. Great physical endurance
Pernicious anemia
1. In absence of intrinsic factor, vitamin B12 is not absorbed
2. Decreased RBC count
3. Treatment- vitamin B12 injections
1. Too few RBCs & platelets & too many WBCs
2. Symptoms- fatigue, frequent infections, bouts of chills & fever, abnormal clotting resulting in bruising & bleeding
3. Treatment- blood transfusions, treating infections & chemotherapy
Drop in plasma proteins alters osmotic pressure sending fluids into the extracellular space
2. Can be a consequence of starvation or protein-deficient diet
Myocardial infarction (heart attack)
1. Blockage of blood vessels feeding the heart
2. Treatment- tissue plasminogen activator (TPA), streptokinase & urokinase break up clots
1. Platelet count below 100,000 per cubic milliliter
2. Excessive bleeding occurs
3. Can be a consequence of radiation treatment, pregnancy, leukemia, cardiac surgery, anemia, infectious disease, bone marrow transplant
4. Treatment- transfusion of platelets or thrombopoietin injections (stimulates production of platelets)
Mature red blood cells are also called 1.-----.
The oxygen-carrying substance in a red blood cell is 1.-----.
a biconcave disc
The shape of a red blood cell can be described as
The shape of a red blood cell can be described as
transporting and exchanging gases (O2 and CO2).
The primary functions of a red blood cell are
Red blood cells with high oxygen concentrations are bright red because of the presence of 1.-----, a particular form of a molecule that is ubiquitious within this cell.
Another name for white blood cells is 1.-----.
granulocytes, agranulocytes
White blood cells with granular cytoplasm are called 1.-----, and white blood cells lacking granular cytoplasm are called 2.-----.
The name, polymorphonuclear leukocyte, describes a specific type of white blood cell, a 1.----- with a segmented nucleus
Normally, the most numerous type of white blood cell are the 1.-----.
1.----- are the type of white blood cell in which the cytoplasmic granules stain red in acid stain
1.----- are normally the least abundant of the white blood cells.
1.----- are the largest of the white blood cells.
1.----- are small agranulocytes that have relatively large, rounded nuclei with thin rims of cytoplasm.
Platelets adhere to rough surfaces, particularly those that occur during injury. When connective tissue is injured, platelets especially adhere to 1.-----, a substance that is found in this tissue.
In the presence of damaged blood vessels, platelets release a substance called 1.----- that causes smooth muscle contraction.
hemocytoblasts , hematopoietic
In red bone marrow, blood cells develop from cells called 1.-----. Another name for these cells is 2.----- stem cells.
red blood cell membranes
Where are the antigens of the ABO blood group located?
How many possible combinations of antigens are there for the ABO blood groups? In other words, the blood of every person contains one of ____ combinations.
Type A blood contains the antigen ____ .
Type B blood contains the antigen ____ .
Type B blood contains antibody ____ in the plasma.
Type A blood contains antibody ____ in the plasma.
both antibodies
Type O blood contains antibody ____ in the plasma
Type AB
Universal recipients is another name for persons with which of these ABO blood types?
Type O
Universal donors is another name for persons with which of these ABO blood types?
2 to 8 months
Alhthough antigens are present at the time of birth, antibodies usually do not appear in the blood until the age of
antigen D
Of the antigens in the Rh group, the most important is
If the red blood cells lack Rh antigens, the blood is called
Rh antibodies form only in persons with ________ type blood in response to special stimulation
If an Rh-negative person who is sensitive to Rh-positive blood receives a transfusion of Rh-positive blood, the donor's cells are likely to
An Rh-negative woman who might be carrying an ________ fetus is given an injection of RhoGAM to prevent erythroblastis fetalis, a hemolytic disease of the newborn.