Chapter 17- Blood Flashcards
1
Q
What are the 3 main functions of blood?
A
- Transport
- Maintenance/regulation
- Protection
2
Q
What substances does blood transport (3)?
A
- Oxygen and nutrient delivery to tissues
- Waste removal from tissues (carbon dioxide and nitrogenous cellular waste)
- Hormone transport to target organs
3
Q
What variables does blood regulate? (3)
A
- Body temperature
- pH
- Fluid volume
4
Q
How does blood regulate body temperature?
A
Blood is mostly water, and water can absorb heat and set the body temperature. Blood can increase or decrease heat also. Blood can be moved closer to or further away from the skin. Blood that is closer to the skin will give off heat.
5
Q
Why is it important for pH to be regulated?
A
pH must stay within its specific range or chemical reactions and cellular functions will be disrupted
6
Q
Why is it important for fluid volume to be regulated?
A
High fluid volume will make your heart work harder, as will low fluid volume- blood must be transported through the body and blood pressure must be maintained.
7
Q
What does blood protect against (2)?
A
- Blood loss- platelets clot blood when blood vessels are damaged
- Infection- leukocytes monitor for pathogens
8
Q
Characteristics of blood (4)
A
- Scarlet to dark red in color, depends on how much oxygen is bound in the red blood cells
- Typical metallic taste due to iron
- pH range: 7.35-7.45
- Viscous- thicker than water due to erythrocyte composition
9
Q
What are the 2 main components of blood?
A
Plasma and blood cells
10
Q
Blood plasma function
A
Transports solutes and suspends the living portion of blood
11
Q
Blood plasma composition
A
90% water, contains many kinds of solutes
12
Q
What types of solutes are present in blood plasma? (6)
A
- Electrolytes
- Nitrogenous substances (urea, uric acid, etc.)
- Organic nutrients (glucose, amino acids, triglycerides, etc.).
- Respiratory gasses- carbon dioxide mainly
- Hormones- don’t enter any cells
- Plasma proteins
13
Q
Plasma proteins
A
This solute makes up most of the mass of blood plasma. They float freely in the plasma, but are not used by cells for energy or nutrients- function varies depending on the protein. One important type of plasma protein is albumin.
14
Q
Where are plasma proteins mainly produced?
A
The liver
15
Q
Albumin
A
Plasma protein that is the major transport protein of blood, contributes to osmotic pressure in capillaries. If you didn’t have albumin, you would lose osmotic pressure.
16
Q
What would happen to the bloodstream if you didn’t produce albumin?
A
A huge amount of water would leave the bloodstream. This is very bad- most of plasma is water, so the heart wouldn’t have much left to pump, it needs water in addition to cells. Water rushes into surrounding body tissues, causing extreme bloating and physically separating cells from each other, disrupting cellular functions because nutrients have a hard time getting to cells
17
Q
Osmotic pressure
A
Osmotic pressure is the measure of the tendency for water to move into a concentrated solution (from the tissues to the blood, for example).
18
Q
Types of blood cells (3)
A
Erythrocytes, leukocytes, platelets. Leukocytes are the only “true” cells since platelets are cell fragments and erythrocytes don’t have organelles.
19
Q
All blood cells are
A
Short lived and non-mitotic- formed by hematopoietic stem cell, so mature cells do not reproduce
20
Q
What is hematocrit? What are the normal ranges for males and females?
A
The portion of total blood volume made up by erythrocytes. Males- 47%, females- 42%
21
Q
Hematopoiesis definition
A
A general term for production of all 3 blood cell types
22
Q
Where does hematopoiesis occur?
A
Red bone marrow tissue.
23
Q
How does hematopoiesis occur?
A
All blood cells arise from hematopoietic stem cells in the bone marrow. Stem cells eventually become “committed” to forming a certain type of blood cell- once committed, the cell cannot become any other cell type. In a single day, the marrow creates about 100 billion new cells. The spleen and liver also destroy a large amount of blood cells every day. This is a balancing act, we don’t want blood to be too thick (have too many cells) or too thin.
24
Q
Where is red bone marrow located?
A
In adults, the axial skeleton, girdles, and heads of femur and humerus. In children, most bones have red bone marrow until they stop growing (18-21).
25
Why don't erythrocytes have a nucleus or other organelles?
This prevents erythrocytes from using the oxygen they are transporting for cellular functions. Therefore, the maximum possible amount of oxygen can be delivered to tissues.
26
How long do erythrocytes typically live?
120 days
27
Hemoglobin
Protein responsible for oxygen transport in the blood, found in erythrocytes
28
Hemoglobin structure
A heme pigment is bound to a globin protein. The heme group has an iron ion at its center- free iron in the body is toxic. Globin has 2 alpha chains and 2 beta chains- each chain binds 1 heme group
29
How many molecules of oxygen can hemoglobin carry?
Each iron center in a heme group can bind one molecule of oxygen, and each hemoglobin has 4 heme groups. Therefore, each hemoglobin can carry 4 oxygen molecules, but red blood cells can carry about a billion oxygen molecules each since they have many hemoglobin molecules.
30
What features make erythrocytes ideal for gas exchange? (3)
1. Large surface area relative to volume increases diffusion rate of oxygen
2. Flattened disc shape increases diffusion rate of oxygen
3. Anaerobic mechanism of energy production- gives the maximum possible amount of oxygen to tissues
31
Erythropoiesis process
Hematopoietic stem cell “commits” to a proerythroblast, which eventually develops into a mature erythrocyte. RBCs retain organelles until the last stage so the nucleus can direct the process.
32
Why does erythropoiesis need to be tightly regulated?
Balance is needed. Too few erythrocytes result in tissue hypoxia, and too many erythrocytes result in viscous blood- the heart is designed to pump blood at a specific viscosity
33
Where is erythropoietin produced?
The kidneys
34
Erythropoietin
A hormone that stimulates erythrocyte production. A small amount is almost always present in the blood to set the basal rate of production.
35
What stimulates erythropoietin production?
Hypoxic conditions in the kidneys cause increased release of EPO. This is a negative feedback mechanism- excessive oxygen supply suppresses EPO release. You release more EPO until oxygen gets too high, then it drops back down. The kidneys don’t care about number of red blood cells, just oxygen availability to cells
36
How does testosterone affect EPO production?
Testosterone enhances production of EPO. It does not stimulate bone marrow directly- stimulates the kidneys. This is why males generally have more erythrocytes and hemoglobin than females.
37
What general substances are necessary for erythropoiesis? (3)
1. General nutrients- amino acids, lipids, carbohydrates necessary for cell synthesis
2. B complex vitamins- B12 and folic acid. Necessary for normal DNA synthesis
3. Iron- necessary for normal hemoglobin synthesis
38
Iron
A mineral that is necessary for normal hemoglobin synthesis. 65% of the body's iron supply is in hemoglobin- the remainder is stored in the liver, spleen, etc..
39
How does iron travel in the blood?
Free iron is toxic, so it binds to protein transferrin- erythrocyte takes up iron as needed. The iron transferrin complex travels in the blood to find a red blood cell, and transferrin detaches so iron can go to the RBC.
40
What happens to erythrocytes as they age?
Hemoglobin begins to degenerate, and the cell becomes less flexible. The cell needs to be flexible to push past each other as they travel through capillaries
41
When erythrocytes break down, how are globin and iron recycled?
Globin is broken down into amino acids and released to circulation. Iron is bound to a transport protein and saved for reuse
42
How are erythrocytes destroyed?
Macrophages engulf and destroy the cell, and the heme group splits free from globin protein. The heme is broken down into bilirubin. It is picked up by the liver, excreted to intestines in bile- leaves body in feces (gives it the brown color). The globin and iron are recycled.
43
Anemia
When there is insufficient oxygen supply to meet body needs. Anemia is just a symptom of another disease or disorder
44
Anemia symptoms
Paleness, cold, shortness of breath, fatigue
45
Causes of anemia (3)
1. Blood loss- acute or chronic hemorrhagic
2. Inadequate erythrocyte production. Example- iron deficiency anemia (nutritional origins), renal anemia (little or no EPO release)
3. Excessive erythrocyte destruction. Example- sickle cell anemia
46
Acute hemorrhagic anemia
Acute hemorrhagic anemia- severe, swift blood loss. Car crash, shooting, stabbing victims
47
Chronic hemorrhagic anemia
Slow, persistent blood loss (ulcer bleeding, hemorrhoids). If you lose blood, you’re also losing blood cells
48
Sickle cell anemia
A genetic condition caused by one amino acid change in the globin chain of erythrocytes. RBCs change their shape to a crescent shape rather than the typical round shape. The hooks of the sickle RBCs hook onto each other and get stuck in blood vessel walls, blocking them, and hemoglobin doesn’t bind and carry oxygen the way they should.
49
Polycythemia
Increase in blood erythrocytes- blood becomes viscous, flows slowly through blood vessels. Heart is basically pumping “sludge”. There are 3 types.
50
Types of polycythemia (3)
1. Polycythemia vera
2. Secondary polycythemia
3. Blood doping
51
Polycythemia vera
A bone marrow cancer- hematocrit levels can get up to 80%. Blood volume doubles, vascular system engorges with blood and impairs circulation. This also puts a lot of stress on blood vessel walls, they become over stretched
52
Polycythemia Vera treatment
Treatment is therapeutic phlebotomy, but the underlying bone marrow cancer has to be treated as well.
53
Secondary polycythemia
Increased EPO release due to low oxygen availability. This is a natural physiological response that occurs at high altitudes. People living in Colorado, for example, produce more erythrocytes.
54
Blood doping
This is used by athletes to increase oxygen carrying capacity during athletic events. This is a temporary type of polycythemia. Too many RBCs make the blood more viscous, which makes the heart work harder. This puts the individual at risk for stroke, heart failure, and many other complications.
55
Methods of blood doping (2)
1. Can take synthetic erythropoietin to stimulate the kidneys like normal
2. Can also take a blood transfusion using their own blood- the blood is withdrawn, they make more blood, then put the old blood back in to increase blood volume
56
Leukocytes general function
Responsible for defending the body
57
Common characteristics of leukocytes (2)
1. Not restricted to the blood vessels- use vessels as transport to certain parts of the body, but can leave if necessary
2. Can be produced very quickly- numbers in the body can double within 2-3 hours
58
Diapedesis
The process by which WBCs can leave vessels via capillary walls
59
Positive chemotaxis
This is how WBCs locate areas of tissue damage/infection/invasion in the body- damaged cells release inflammatory chemicals to attract WBCs
60
Two major categories of leukocytes
Granulocytes and agranulocytes
61
Granulocytes
A type of leukocyte that is spherical in shape. These are large, short lived cells packed with granules
62
Types of granulocytes (3)
1. Neutrophils
2. Eosinophils
3. Basophils
63
Neutrophils
Bacteria killer cells that are 50-70% of the total leukocyte population. Contain defensins- antimicrobial protein that kills off bacteria. Chemically attracted to sites of inflammation, can phagocytize
64
Defensins
Antimicrobial proteins that kill off bacteria by punching holes in their membrane. Water rushes into the bacterial cell, so it eventually explodes and dies
65
Eosinophils
Parasite killer cells, 2-4% of the leukocyte population. Lysosomes in the cell contain digestive enzymes- they will digest invading parasites by breaking down their body wall
66
Basophils
0.5-1% of the leukocyte population, contain histamine-containing granules- associated with allergic reactions. Large numbers of basophils make allergic reactions more likely and more severe
67
Histamine
Histamines cause the symptoms of allergic reactions- histamine release causes vasodilation, attracts other leukocytes to an area
68
Agranulocytes
Leukocytes that lack visible granules
69
Types of agranulocytes (2)
1. Lymphocytes
| 2. Monocytes
70
Lymphocytes
25% of the leukocyte population. Not found in blood- mostly in lymphoid tissue- only migrate out if there’s something they need to destroy. There are 2 types.
71
Types of lymphocytes (2)
1. B-lymphocytes
| 2. T-lymphocytes
72
T-lymphocytes
Act against virus infected cells and tumor cells
73
B-lymphocytes
Produce antibodies released to blood. They will flag a pathogen as something that doesn’t belong.
74
Monocytes
3-8% of leukocyte population. Differentiate into macrophages as they leave bloodstream and enter tissue. They are actively phagocytic- destroy bacteria, viruses, sources of chronic infection
75
Leukopoiesis definition
Production of leukocytes
76
What 2 chemical messengers stimulate leukopoiesis?
1. Interleukins
2. Colony-stimulating factors
These chemical messengers can act as either paracrines or hormones. They are glycoproteins that stimulate specific leukocyte populations.
77
What 2 leukocyte pathways can hematopoietic stem cells differentiate into?
1. Myeloid stem cell
| 2. Lymphoid stem cell
78
Myeloid stem cell
Commits to either myeloblast (eventually forms eosinophil, basophil, or neutrophil) or monoblast (eventually forms monocytes)
79
Lymphoid stem cell
Commits to either B-lymphocyte or T-lymphocyte precursor cells. Precursor cells mature to a B-lymphocyte or T-lymphocyte
80
What is leukemia?
Cancer resulting in over-production of abnormal (nonfunctional) leukocytes. Cells originate from a single abnormal cell. Abnormal leukocytes remain unspecialized and proliferate extensively.
81
Complications of leukemia
Abnormal leukocytes do not defend the body- infections, hemorrhage occur. Cancerous leukocytes crowd red marrow, and immature leukocytes flood the bloodstream. Therefore, other blood cells are crowded out of blood- anemia, bleeding problems (platelets)
82
How is leukemia named?
According to how fast cells proliferate (acute/chronic) and the type of cell involved (lymphocytic/myeloid). These two things are combined to name the disease (acute lymphocytic, chronic myeloid, etc.).
83
Acute leukemia
Derived from hematopoietic stem cells and proliferates quickly. Primarily affects children
84
Chronic leukemia
Derived from later cell stages, primarily affects the elderly
85
Myeloid leukemia
Involves myeloid stem cell descendants- any granulocytes and monocytes
86
Lymphocytic leukemia
Involves lymphocytes
87
Infectious mononucleosis
The “kissing disease”, aka mono. This is a viral disease caused by the Epstein-Barr virus that mostly affects younger or college age individuals. Results in a high number of large and atypical lymphocytes
88
Infectious mononucleosis symptoms
Low grade fever, fatigue, body soreness, sore throat
89
Infectious mononucleosis treatment
None, you just have to wait it out. Recovery can take at least 3-4 weeks but possibly even longer, it's 4-6 weeks on average
90
What are platelets?
Fragments of large cells (megakaryocytes) that are short lived- only last about 10 days if unused. They initiate blood clot formation after injury to blood vessel wall. When blood vessel wall is damaged/torn, platelets stick to each other and to injury site. They have “arms” that attach to other platelets
91
What prevents platelets from sticking together when a blood vessel isn't damaged?
When there is no damage, prostacyclin and nitric oxide prevent platelets from sticking together. These molecules are secreted by endothelial cells lining the blood vessels. A blot clot without injury would impair circulation.
92
What regulates platelet formation?
A hormone called thrombopoietin.
93
Hemostasis
The process by which bleeding is stopped after blood vessel rupture occurs. This is a localized response that progresses very quickly
94
3 steps involved in hemostasis
1. Vascular spasm
2. Platelet plug formation
3. Coagulation
95
What occurs during vascular spasm?
Rapid constriction of an injured blood vessel. This is triggered by injured smooth muscle tissue, chemicals released by damaged endothelial cells of vessel wall, and reflexes from local pain receptors.
96
Vascular spasm benefits
Constricting damaged vessel causes less blood to flow through them- initially decreases blood loss
97
What occurs during platelet plug formation?
Platelets stick together to form a plug in damaged blood vessel. They also stick to exposed collagen fibers in damaged endothelium.
98
What do platelets release in response to injury to form a positive feedback mechanism during platelet plug formation? (2)
1. ADP- causes more platelets to stick to the site of injury
| 2. Serotonin, thromboxane A2- increase vascular spasm and platelet aggregation- creates a thicker plug
99
What are platelet plugs used for?
Platelet plugs are only good for general wear and tear and small injuries- general wear and tear are the small amount of damage to blood vessels that occurs just by moving around. Larger injuries require a more severe mechanism to stop bleeding.
100
Coagulation
This is the formation of blood clots with fibrinogen, used more often for large tears/breaks. Blood proteins form fibrin strands that link together- form tough meshwork
101
Coagulation process (3 general steps)
1. Series of clotting factors (I-XIII) involved to form prothrombin activator
2. Prothrombin activator catalyzes conversion of plasma protein prothrombin into the active enzyme thrombin.
3. Thrombin catalyzes the transformation of soluble clotting factor fibrinogen into fibrin.
102
Where are clotting factors made?
The liver
103
What does fibrin do during coagulation?
Fibrin molecules link together to form long, insoluble strands that stick together. The strands trap platelets together, forming a true blood clot. Anything that tries to pass through (RBCs, etc.) get trapped in mesh
104
Factor XIII
Fibrin stabilizing factor- this is an enzyme that binds fibrin strands to one another. Provides strength to blood clot- resists stretching/tearing of fibrin molecules
105
Blood clot retraction definition
The process of pulling damaged edges of blood vessels close together
106
What occurs during blood clot retraction?
Platelets in blood clot have contractile ability- contraction pulls fibrin strands together, squeezing out serum fluids and pulling edges of injury closer together. This makes the blood clot thicker and stronger so it won’t tear away as easily
107
Platelet-derived growth factor
Causes increase in number of fibroblasts and smooth muscle cells in damaged area, and forms connective tissue that will eventually form new blood vessel wall during blood clot retraction
108
Fibrinolysis definition
The removal of a blood clot after healing is complete
109
What occurs during fibrinolysis
Clotting factors and thrombin activate plasmin enzyme- activity confined to clot. Importance- without this process, blood vessels become permanently blocked over time. Typically begins within 2 days of clot formation.
110
Thromboembolic disorders
Formation of undesirable blood clots
111
Thrombus
Formation of blood clot in unbroken vessel (remains stuck to vessel wall). Effect- blocks blood circulation. For example, coronary circulation blockage leads to heart tissue failure, death
112
Embolus
Thrombus that enters circulation. Effect: if small, embolus generally isn’t a problem, but if large, it can obstruct smaller blood vessels and block circulation. Ex- pulmonary embolism, cerebral embolism
113
Anticoagulant drugs
Used to treat undesirable clotting. Aspirin, heparin, and warfarin are examples.
114
Aspirin
Blocks platelet aggregation and plug formation. Taking low dose aspirin daily may decrease risk of heart attack in older individuals
115
Heparin
Used to prevent clot formation in hospitals for surgical procedures
116
Warfarin
Prevents production of certain clotting factors
117
Thrombocytopenia
Low number of platelets in circulation. This causes a limited ability of the body to form platelet plugs- even “small breaks” can cause massive hemorrhage. Causes- usually anything that decreases red bone marrow will decrease platelet count
118
Hemophilia
A group of hereditary bleeding disorders. Deficiency or absence of certain clotting factors causes extreme bleeding from small cuts/injuries. Treatment- plasma transfusions, injections of clotting factor. Includes hemophilia A, B, and C.
119
Hemophilia symptoms
Prolonged bleeding into tissues, painful/disabled joints. Damaged blood vessels surrounding joints causes bleeding into the joints
120
Hemophilia A
Deficiency of clotting factor VIII
121
Hemophilia B
Deficiency of clotting factor IX
122
Hemophilia C
Lack of factor XI, the most mild of the 3 forms
123
How does the body compensate for blood loss? (2)
1. Decreasing blood volume to injured blood vessels
| 2. Increasing red blood cell production by red bone marrow
124
How much blood loss is problematic?
Losing 15-30% of total blood volume leads to weakness, 30% and higher can lead to severe shock and possibly death. The body can only compensate so much
125
When are whole blood transfusions used?
Whole blood transfusions are rare. They're only necessary when large volumes of blood are lost, and are usually a last resort. More often, red cell transfusions are used
126
Antigens
Antigens are cellular identifiers, WBCs use it to determine if the cell should be in your body or not. These are the extracellular markers on erythrocytes. Also called agglutinogens.
127
What happens during a transfusion reaction?
Antibodies (agglutinins) attack “foreign” donor blood cells. Foreign erythrocytes are clumped together, blocking blood vessels. Blood cells will eventually start to lyse- release hemoglobin to blood stream. Causes decreased oxygen transport and hemoglobin passes freely into kidney tubules- kidney shutdown
128
ABO blood groups (4)
1. Blood type A- cells have “A” antigen
2. Blood type B- cells have “B” antigen
3. Blood type O- cells do not have any antigen
4. Blood type AB- cells have both “A” and “B” antigen
129
Agglutinins
Antibodies that will act against an antigen that is not present on a person’s own blood cells
130
What agglutinins does each blood type have?
1. A person with type A blood has anti-B agglutinins.
2. A person with type B blood has anti-A agglutinins.
3. A person with type AB blood has neither type of antibody
4. A person with type O blood has both anti-A and anti-B antibodies
131
Rh blood groups
Five antigens make up this blood group- C, D, E, c, and e. If you carry the D antigen, you are Rh+. If you do not carry the D antigen (C, E, c, or e), you are Rh-
132
What happens if Rh blood groups are mismatched?
Rh- will create antibodies (have a reaction) if mismatched. Rh- can’t get Rh+, but Rh+ can get Rh-
133
Which blood type is the "universal donor"?
Type O. Neither antigen is present on blood cell surface. Antibodies in the recipient body have no basis to judge “foreign” vs. “not foreign”. Problem- type O has both antibodies- can only accept type O blood transfusion
134
Which blood type is the "universal recipient"?
Type AB. Neither antibody is present, so there's nothing to attack “foreign” red blood cells.
135
What are the risk factors for thromboembolic disease?
1. Atherosclerosis or inflammation- this roughens the vessel endothelium and allows platelets to take hold
2. Slowly flowing blood, like when a person is bedridden or taking a long flight without moving around. Clotting factors are not washed away as usual and accumulate- clots can form
136
Blood chemistry tests
Chemical analysis of substances in the blood (glucose, iron, calcium, protein, bilirubin, and pH
137
Blood fraction
Any one of the components of whole blood that has been separated from the other blood components, such as platelets and clotting factors
138
Bone marrow biopsy
A sample of red bone marrow is obtained by needle aspiration (typically from the anterior or posterior iliac crest) and examined to diagnose disorders of blood cell formation, leukemia, various marrow infections, and anemias resulting from damage to or failure of the marrow.
139
Exchange transfusion
A technique of removing the patient's blood and infusing donor blood until a large fraction of the patient's blood has been replaced- used to treat fetal blood incompatibilities and poisoning victims
140
Hematoma
Accumulated, clotted blood in the tissues usually resulting from injury, visible as marks or bruises. Eventually absorbed naturally unless infections develop.
141
Hemochromatosis
An inherited disorder of iron overload in which the intestine absorbs too much iron from the diet. The iron builds up in body tissues, where it oxidizes to form compounds that poison those organs (especially joints, liver, and pancreas).
142
Myeloproliferative disorders
A broad term for a group of proliferative disorders (disorders in which normal cell division controls are lost) includes leukoerythroblastic anemia involving fibrosis of the bone marrow, polycythemia vera, and leukemia
143
Plasmapheresis
A process in which the blood is removed, its plasma is separated from formed elements and the formed elements are returned to the patient or donor. Usually used for removal of antibodies or immune complexes from the blood of individuals with autoimmune disorders (multiple sclerosis)
144
Septicemia
Excessive and harmful levels of bacteria or their toxins in the blood. Also called blood poisoning
145
Treatments for sickle cell anemia
Nitric oxide dilates blood vessels to give sickles more room, and a bone marrow transplant can potentially be a cure in children who have had multiple complications from the disease.
