Chapter 19: Cardiovascular System and Blood Flashcards
1
Q
Which 3 interrelated components make up the cardiovascular system?
A
Blood, heart, blood vessels.
2
Q
Blood.
A
Liquid connective tissue. Cells surrounded by a liquid extracellular matrix (plasma) which suspends cells and cell fragments.
3
Q
Interstitial fluid.
A
Fluid that bathes body cells and is constantly renewed by blood.
4
Q
What are the 3 functions of blood?
A
Transportation, regulation and protection.
5
Q
What is the blood’s role in transportation?
A
Transports O2 from lungs to body cells. Transports CO2 from body cells to lungs. Transports nutrients from GI to body cells. Transports hormones from endocrine glands to body cells. Transports heat and waste to organs for elimination.
6
Q
What is the blood’s role in regulation?
A
Maintains homeostasis, regulates pH levels using buffers, adjusts body temperature using water in plasma, regulates osmotic pressure, regulates water content of cells.
7
Q
What is the blood’s role in protection?
A
Clotting decreases blood loss after an injury, WBCs protect against disease-carrying pathogens, and blood proteins protect against disease.
8
Q
What is the average blood volume of an adult male and an adult female?
A
Male: 5-6 L. Female: 4-5 L.
9
Q
What are the components of blood?
A
55% blood plasma. 45% formed elements.
10
Q
Describe centrifuged blood.
A
Bottom: cells. Middle: buffy coat (WBCs, platelets). Top: plasma.
11
Q
Blood plasma components.
A
Watery liquid ECM containing dissolved substances. 91.5% water. 8.5% solutes (electrolytes, enzymes, hormones, gases, waste).
12
Q
Formed elements components.
A
Cells and cell fragments. 99% RBCs. 1% WBCs and platelets.
13
Q
Hepatocytes synthesize which cells to make plasma proteins?
A
Albumins: 54%. Globulins: 38%. Fibrinogen: 7%.
14
Q
Gamma globulins.
A
Antibodies. Plasma proteins.
15
Q
Hematocrit.
A
The percentage of total blood volume occupied by RBCs.
16
Q
What is the normal range of hematocrit for adult males and for adult females?
A
Males: 40-54%. Females: 38-46%.
17
Q
Which hormone stimulates the production of RBCs, and stimulates its synthesis:
A
Erythropoietin. Stimulated by testosterone.
18
Q
A significant drop in hematocrit indicates:
A
Anemia.
19
Q
Polycythemia.
A
Indicates an abnormally high RBC count, with a hematocrit of 65%+. Increased viscosity, resistance to flow, BP, risk of stroke. Causes: RBC production increase, tissue hypoxia, dehydration, blood doping, athletic EPO use.
20
Q
Platelets.
A
Fragments of cells without a nucleus. Release chemicals to promote blood clotting when vessels are damaged.
21
Q
Thrombocytes.
A
Functionally equivalent to platelets. Nucleated cells found in lower vertebrae.
22
Q
What is responsible for regulating the number of RBCs and platelets in circulation.
A
Negative feedback.
23
Q
Which component of formed elements varies in abundance?
A
WBCs. Due to invading pathogens and foreign antigens.
24
Q
Hemopoiesis.
A
Process by which formed elements develop. Before birth, it occurs in the yolk sac of an embryo and later in the liver, spleen, thymus and lymph nodes of fetus. Red bone marrow then becomes the primary site in the last 3 months before birth and throughout life.
25
Red bone marrow.
Highly vascularized connective tissue. Located between trabeculae of spongy bone tissue. Present in bones of axial skeleton, pectoral girdle, pelvic girdle, and proximal epiphyses of humerus and femur.
26
Describe red and yellow bone marrow throughout a lifetime.
In newborns, all bone marrow is red and active in blood cell production. As an individual ages, the rate of blood cell production decreases. Red bone marrow in medullary cavity of long bones becomes inactive and is replaced by yellow bone marrow.
27
What can happen to yellow bone marrow during severe bleeding?
It can revert back to red bone marrow. Blood-forming stem cells from red bone marrow move into yellow bone marrow, which is then repopulated by pluripotent stem cells.
28
Pluripotent stem cells.
Hemocytoblasts. >1% of red bone marrow cells. Derived from mesenchyme.
29
Reticular cells.
Produce reticular fibres, which form the stroma that supports red bone marrow cells.
30
Formed elements do not divide once they leave red bone marrow, except for which cell?
Lymphocytes.
31
Pluripotent stem cells in red bone marrow produce 2 types of stem cells:
Myeloid stem cells: give rise to RBCs, platelets, monocytes, neutrophils, eosinophils, basophils, mast cells. Lymphoid stem cells: give rise to lymphocytes and NK cells.
32
Where do the myeloid stem cells and lymphoid stem cells begin their development?
Myeloid: red bone marrow. Lymphoid: red bone marrow --> lymphatic tissues.
33
What is the histological appearance of stem cells and progenitor cells?
They cannot be distinguished histologically, and they both resemble lymphocytes.
34
Progenitor cells.
Derived by some myeloid stem cells. They are no longer capable of reproducing themselves, and are committed to giving rise to more specific elements of blood.
35
Colony-forming units (CFUs).
Some progenitor cells are known as CFUs. CFU-E: produces RBCs. CFU-Meg: produces megakaryocytes. CFU-GM: produces granulocytes and monocytes.
36
After progenitor cell, the next generation of cells are called:
Precursor cells (blasts). Have recognizable microscopic appearances.
37
Erythropoietin (EPO).
Increases the number of RBC precursor cells. Produced by kidney cells. Renal failure --> decreased EPO release --> decreased RBC production --> decreased hematocrit --> decreased ability to deliver oxygen throughout body.
38
Thrombopoietin (TPO).
Stimulates the formation of platelets from megakaryocytes. Produced by liver cells.
39
What regulates the development of different blood types?
Cytokines.
40
Cytokines.
Small glycoproteins that act as local hormones. Stimulate proliferation of progenitor cells in red bone marrow and regulate the activities of cells involved in nonspecific defences and immune responses.
41
Hemoglobin.
Pigment that gives blood its red colour. Oxygen-carrying protein. Each RBC contains 280 million hemoglobin molecules. Transports 23% of all CO2. Regulates blood flow and BP.
42
How many RBCs are in an average adult male and an adult female?
Male: 5.4 million per microlitre of blood. Female: 4.8 million per microlitre of blood.
43
To maintain normal numbers of RBCs, new mature cells must enter the circulation at what rate?
2 million per second.
44
Describe a RBC.
Plasma membrane is strong and flexible, allowing it to deform without rupturing when moving through vessels. No nucleus. No organelles. Cannot reproduce or carry on extensive metabolic activities. Cytosol contains hemoglobin molecules. All internal space is available for oxygen transport. They do not use any of the oxygen they transport. Their shape maximizes surface area for diffusion of gas molecules.
45
Describe a hemoglobin molecule.
Consists of a global protein composed of 4 polypeptide chains, with a ringlike heme pigment bound to each of the 4 chains. At the centre of each heme ring is an Fe that can combine reversibly with an O2, allowing each hemoglobin molecule to bind 4 O2 molecules. Each O2 molecule picked up from the lungs is bound to an Fe --> as blood flows through tissue capillaries the Fe-O2 reaction reverses --> hemoglobin releases O2 --> O2 diffuses into interstitial fluid and into cells.
46
How is some CO2 transported back to the lungs for exhalation by hemoglobin?
Blood flowing through tissue capillaries picks up CO2 --> some combines with amino acids in globin part of hemoglobin --> CO2 is released from hemoglobin in the lungs.
47
How does hemoglobin regulate blood flow and BP?
Endothelial cells of blood vessels produce NO --> binds to hemoglobin --> releases NO under certain conditions --> causes vasodilation --> improves blood flow and enhances oxygen delivery.
48
Carbonic anhydrase (CA).
Catalyzes the conversion of CO2 and H2O to carbonic acid which dissociates into H+ and HCO3-. Allows 70% of CO2 to be transported in blood plasma from tissue cells to lungs as HCO3-. Serves as an important buffer in ECF.
49
How long do RBCs typically live for?
120 days. Wear and tear.
50
Describe the life cycle of a RBC.
Macrophages in spleen, liver and red bone marrow phagocytize ruptured and worn-out RBCs --> globin and heme are split apart --> globin is broken down into amino acids which can be reused to synthesize other proteins --> Fe is removed from heme which associates with transferrin --> in muscle fibres, liver cells and macrophages of spleen and liver, Fe detaches from transferrin and attaches to ferritin --> on release from a storage site or absorption from GI tract, Fe reattaches to transferrin --> complex is carried to red bone marrow where RBC precursors take it up through receptor-mediated endocytosis for use in hemoglobin synthesis (Fe is needed for heme part, amino acids are needed for globin part, vitamin B12 is needed) --> erythropoiesis in red bone marrow results in RBC production --> enter circulation --> when Fe is removed from heme, the non-Fe part of heme is converted to biliverdin and then into bilirubin --> bilirubin enters blood and goes to liver --> released by liver cells --> bile --> small intestine and large intestine --> bacteria convert bilirubin into urobilinogen --> some is absorbed back into blood, converted to urobilin and excreted in urine --> most is eliminated in feces as stercobilin.
51
Transferrin.
Plasma protein. Transporter for Fe in the blood.
52
Ferritin.
Protein that stores Fe.
53
What is biliverdin and bilirubin?
Biliverdin: green pigment. Bilirubin: yellow-orange pigment.
54
What is urobilin and stercobilin?
Urobilin: yellow pigment, urine. Sterobilin: brown pigment, feces.
55
Describe the process of erythropoiesis.
Proerythroblast in red bone marrow --> divides many times --> produces cells that synthesize hemoglobin --> a cell near the end of the development sequence ejects its nucleus and becomes a reticulocyte --> centre of cell indents producing a biconcave shape --> reticulocytes retain some mitochondria, ribosomes, ER --> pass from red bone marrow to blood by squeezing between PMs of endothelial cells of blood capillaries --> develop into mature RBCs within 1-2 days after their release from red bone marrow.
56
Hypoxia.
Oxygen deficiency at tissue level. May occur if too little oxygen enters the blood, which can be caused by anemia or circulatory problems. Stimulates the kidneys to increase EPO release --> proerythroblasts --> reticulocytes --> RBCs.
57
Causes of anemia.
Low Fe, amino acids, vitamin B12.
58
Why do premature newborns often exhibit anemia?
Inadequate production of EPO, since the liver produces most EPO during the first few weeks after birth, and the liver is less sensitive than the kidneys to hypoxia. Fetal hemoglobin also carries 30% more oxygen, so the loss of this fetal hemoglobin makes the anemia worse.
59
WBCs.
Have a nucleus and organelles.
60
Granular leuokocytes.
Neutrophils, eosinophils, basophils. Display conspicuous granules with distinctive coloration.
61
Neutrophil.
Small granules are evenly distributed and are neutrophilic. Pale lilac colour. Older neutrophils are called polymorphonuclear leukocytes (PMNs). Respond most quickly to tissue destruction by bacteria. After engulfing a pathogen, the neutrophil releases chemicals to destroy it. Contain defensins, which have antibiotic activity against bacteria and fungi, and form peptide spears to poke holes in microbe membranes.
62
Eosinophil.
Large granules do not cover the nucleus, and they stain red-orange with acidic dye. Release histaminase to combat histamine effects, and other substances involved in inflammation during allergic reactions. Phagocytize antigen-antibody complexes. Effective against parasitic worms.
63
Basophil.
Round granules obscure the nucleus, and they stain blue-purple with basic dye. Release granules that contain heparin, histamine and serotonin to intensify the inflammatory reaction. Involved in hypersensitivity and allergic responses. Similar in function to mast cells.
64
Agranular leukocytes.
Lymphocytes and monocytes. Granules are not visible under the microscope because of their size and poor staining qualities.
65
Lymphocyte.
Round nucleus that stains dark. Cytoplasm forms a ring around nucleus and stains light blue. Large = 10-14 um diameter. Small = 6-9 um diameter. Major soldiers in lymphatic system battles. B-cells: effective in destroying bacteria and inactivating their toxins. T-cells: attack infected body cells and tumour cells, and are responsible for the rejected of transplanted organs. NK-cells: attack infected body cells and tumour cells.
66
Monocyte.
Kidney- or horseshoe-shaped nucleus. Cytoplasm is foamy and stains blue-grey. Fixed = remain in a tissue. Wandering = roam tissues and gather at sites of infection/inflammation. Take longer to reach infection site, but arrive in large numbers and destroy more microbes. They enlarge and differentiate into wander macrophages, which clean up cellular debris and microbes by phagocytosis after an infection.
67
MHC antigens.
Present in WBCs and all other nucleated cells in the body. Protrude from PM into ECF. Unique for each person except for identical twins.
68
Ratio of RBCs:WBCs.
700:1
69
Leukocytosis.
Increased WBC count above 10,000 per microlitre of blood. Normal protective response to stress.
70
Leukopenia.
Decreased WBC count below 5,000 per microlitre of blood. May be caused by radiation, shock, or chemotherapy drugs.
71
WBC function.
Combat pathogens by phagocytosis or immune responses. Many WBCs leave the bloodstream and collect at sites of pathogen invasion or inflammation.
72
Which WBCs never return to the bloodstream, once leaving to fight injury or infection?
Granular leukocytes and monocytes.
73
Which WBC continually recirculates from the blood to interstitial spaces of tissues to lymphatic fluid and back to the blood?
Lymphocytes.
74
How do WBCs leave the bloodstream?
Emigration. WBCs roll along the endothelium, stick to it, and then squeeze between endothelial cells.
75
Which molecules help WBCs stick to the endothelium?
Adhesion molecules. Selectins: stick to CHO on the surface of neutrophils to help them roll along the endothelial surface. Integrins: tether neutrophils to the endothelium and assist their movement through the blood vessel walls and into the interstitial fluid of the injured tissue.
76
Which WBCs participate in phagocytosis?
Neutrophils and macrophages. They ingest bacteria and dispose of the dead matter. Chemotaxis attracts phagocytes.
77
High eosinophil count:
Allergic reaction or parasitic infection.
78
Differential WBC count.
A count for each of the 5 types of WBCs. Detects infection, inflammation, drug poisoning, blood disorders, chemotherapy side effects, allergic reactions, parasitic infections.
79
Platelets.
Break off from the megakaryocytes in red bone marrow and enter blood circulation. No nucleus. Irregular disc-shape. Many vesicles. Granules contain chemicals that promote blood clotting. Form platelet plug. Short life span (5-9 days). Aged and dead platelets are removed by fixed macrophages in spleen and liver. Store clotting factors, ADP, ATP, calcium, serotonin, enzymes that produce thromboxane A2 and prostaglandin, lysosomes, mitochondria, membrane systems, glycogen, PDGF.
80
Under the influence of TPO, myeloid stem cells develop into:
Megakaryocyte colony-forming cells --> megakaryoblasts --> megakaryocytes --> splinter into 2000-3000 fragments (platelets).
81
Hemostasis.
Quick sequence of responses that stops bleeding when blood vessels are damaged. Carefully controlled. Localized to the region of damage. Prevents hemorrhage.
82
Vascular spasm.
When arteries or arterioles are damaged, the circularly arranged smooth muscle in their walls contracts immediately to reduce blood loss for several minutes to hours. The spasm is caused by damage to the smooth muscle, by substances released from activated platelets, and by reflexes initiated by pain receptors.
83
Platelet plug formation.
Effective in preventing blood loss in a small vessel. Becomes reinforced by fibrin threads formed during clotting. Can completely stop blood loss if the hole in the vessel is not too large.
84
Platelet plug formation steps.
Platelets contact and stick to parts of a damaged blood vessel (platelet adhesion) --> platelets become activated and their characteristics change due to adhesion --> they extend many projections that enable them to contact and interact with one another and they begin to liberate the contents of their vesicles (platelet release reaction) --> liberated ADP and thromboxane A2 activate nearby platelets --> 5HT and thromboxane A2 function as vasoconstrictors, which decreases blood flow through injured vessel --> ADP makes other platelets in the area sticky --> stickiness of platelets causes them to adhere to the originally activated platelets (platelet aggregation) --> platelet plug.
85
Serum.
Straw-coloured liquid. Blood plasma without the clotting proteins.
86
Blood clot.
Gel. Consists of a network of fibrin in which the formed elements of blood are trapped.
87
Clotting/coagulation.
Process of gel formation. Series of chemical reactions that culminates in formation of fibrin threads.
88
Thrombosis.
Can be caused by blood clotting too easily. Can result in clotting in undamaged vessels. Thrombus (clot) may dissolve spontaneously, but it could also be swept away in the bloodstream.
89
Hemorrhage.
Can be caused by blood taking too long to clot.
90
Clotting factors.
Calcium, inactive enzymes synthesized by hepatocytes and released into blood, various molecules associated with platelets or released by damaged tissue. Most clotting factors are identified by Roman numerals that indicate the order of their discovery.
91
Blood clotting.
Complex cascade of enzymatic reactions in which each clotting factor activates many molecules of the next one in a fixed sequence. Produces a lot of fibrin.
92
Describe the process of blood clotting.
Extrinsic pathway and intrinsic pathway --> prothrombinase --> converts prothrombin to thrombin --> converts soluble fibrinogen to insoluble fibrin --> forms threads of clot.
93
Extrinsic pathway.
Occurs within seconds if trauma is severe. Tissue factor leaks into blood from cells outside blood vessels --> begins a sequence of reactions that activates clotting factor X in presence of calcium --> combines with factor V in presence of calcium --> prothrombinase.
94
Tissue factor (TF).
Thromboplastin. Complex mixture of lipoproteins and phospholipids released from surfaces of damaged cells.
95
Intrinsic pathway.
Occurs slowly over several minutes. Its activators are either in direct contact with blood, or contained within the blood. If endothelial cells become roughened or damaged, blood can come into contact with collagen fibres in the connective tissue around the endothelium of the blood vessel. Trauma to endothelial cells causes damage to platelets, resulting in the release of phospholipids. Contact with collagen fibres activates clotting factor XII --> begins sequence of reactions that activates clotting factor X --> platelet phospholipids and calcium also participate in clotting factor X activation --> combines with factor V --> prothrombinase.
96
Common pathway.
Prothrombinase and calcium catalyze the conversion of prothrombin to thrombin --> thrombin converts fibrinogen to fibrin in the presence of calcium --> thrombin also activates factor XIII which strengthens and stabilizes the fibrin threads into a sturdy clot. Plasma contains factor XIII which is also released by platelets trapped in the clot.
97
Thrombin has 2 positive feedback effects:
1) Accelerates the formation of prothrombinase --> accelerates production of thrombin.
2) Activates platelets --> reinforces aggregation and release of platelet phospholipids.
98
Clot retraction.
Consolidation/tightening of the fibrin clot. Fibrin threads attached to the damaged blood vessel contract as platelets pull on them, pulling the edges of the damaged vessel closer together to decrease the risk of further damage. Serum can escape between the fibrin threads, but the formed elements cannot. After this, permanent repair of the blood vessel can occur (fibroblasts form connective tissue in the ruptured area and new endothelial cells repair the vessel lining).
99
Clot retraction depends on:
An adequate number of platelets in the clot, which releases factor XIII to strengthen and stabilize the clot.
100
Role of vitamin K in blood clotting.
Required for the synthesis of 4 clotting factors. Vitamin K is normally produced by bacteria in the large intestine, and is a fact-soluble vitamin that can be absorbed through the lining of the intestine and into the blood. People suffering from slow absorption of lipids often experience uncontrolled bleeding as a consequence of vitamin K deficiency.
101
Fibrinolytic system.
Dissolves small inappropriate clots that form during the course of a regular day, and clots at a site of damage once the damage is repaired.
102
Fibrinolysis.
Dissolution of a clot.
103
Plasminogen.
When a clot is formed, inactive plasminogen is incorporated into the clot. Tissues and blood contain substances that can activate plasminogen to plasmin. Plasmin can dissolve the clot by digesting fibrin threads and inactivating certain substances. A clot does not extend beyond a wound site into the general circulation because fibrin absorbs thrombin in the clot, and because clotting factor concentrations are not high enough to produce widespread clotting.
104
Prostacyclin.
A prostaglandin produced by endothelial cells and WBCs. Opposes the actions of thromboxane A2. Powerful inhibitor of platelet adhesion and release.
105
Anticoagulants.
Delay, suppress and prevent blood clotting. Antithrombin: blocks factors XII, X, II. Heparin: produced by mast cells and basophils, and combines with antithrombin to increase it effectiveness in blocking thrombin. APC: inactivates the 2 major clotting factors not blocked by antithrombin, and enhances activity of plasminogen activators.
106
What happens to babies that are unable to produce APC due to genetic mutation?
Die of blood clots in infancy.
107
Intravascular clotting.
Blood clots sometimes form within the cardiovascular system. May happen when blood flows too slowly, or due to atherosclerosis, trauma, infection.
108
Embolus.
Blood clot, air bubble, fat from broken bone, or a piece of debris transported by the bloodstream.
109
Pulmonary embolism.
When an embolus lodges in the lungs.
110
The surfaces of RBCs contain a genetically determined assortment of antigens composed of:
Glycoproteins and glycolipids. These antigens occur in characteristic combinations. Blood is categorized into different blood groups based on the presence or absence of certain antigens.
111
Within a blood group, there can be:
More than 2 different blood types.
112
Two major blood groups.
ABO and Rh.
113
ABO blood group.
Based on two glycolipid antigens: A and B. Type A: RBCs with only antigen A. Type B: RBCs with only antigen B. Type AB: RBCs with both antigens A and B. Type O: RBCs with neither antigens A or B.
114
Blood plasma contains antibodies (agglutinins) that react with A or B antigens:
Anti-A antibody reacts with antigen A. Anti-B antibody reacts with antigen B. These antibodies are large IgM-type that do not cross the placenta, so they rarely cause problems for mother and fetus.
115
Blood transfusions.
Transfer of whole blood or blood components into bloodstream or red bone marrow.
116
In an incompatible blood transfusion:
Antibodies in the recipients plasma bind to the antigens on the donated RBCs --> agglutination/clumping of RBCs --> RBCs become cross-linked to one another --> activate complement molecules that make the PM of the donated RBCs leaky --> hemolysis/rupture of RBCs --> hemoglobin is released into blood plasma --> kidney damage (clog filtration membranes).
117
Universal recipients.
Type AB. Do not have anti-A or anti-B antibodies.
118
Rh blood group.
Rh+: RBCs have Rh antigens. Rh-: RBCs lack Rh antigens. The alleles of 3 genes may code for the Rh antigen. If an Rh- person receives an Rh+ blood transfusion, the immune system starts to make anti-Rh antibodies that will remain in the blood. If a second transfusion of Rh+ is given later, the previously formed anti-Rh will cause agglutination and hemolysis of donated RBCs.
