The Cardiovascular System: The Blood, Heart, & Blood Vessels
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1 The Cardiovascular System: The Blood, Heart, & Blood Vessels
2 Fluids of the Body Cells of the body are serviced by 2 fluids 1. Blood a liquid connective tissue that consists of cells surrounded by a liquid extracellular matrix. 2. Interstitial fluid the fluid that bathes body cells and is constantly renewed by the blood Nutrients and oxygen diffuse from the blood into the interstitial fluid & then into the cells Wastes move in the reverse direction Hematology is study of blood and blood disorders
3 Functions of Blood 1.Transportation O 2, CO 2, metabolic wastes, nutrients, hormones, nutrients 2. Regulation helps regulate ph through buffers helps regulate body temperature coolant properties of water vasodilatation of surface vessels removes heat from interior helps regulate water content of cells by interactions with dissolved ions and proteins - osmosis 3.Protection from disease & loss of blood
4 Physical Characteristics of Blood Thicker (more viscous) than water and flows more slowly than water - 8% of body weight Temperature of o F ph 7.4 ( ) - metabolic acidosis vs. metaoblic alkalosis Color is bright red when saturated with O 2 and dark red when unsaturated Blood volume 5 to 6 liters in average male 4 to 5 liters in average female
5 Venipuncture Techniques of Blood Sampling sample taken from vein with hypodermic needle & syringe Finger or heel stick common technique for diabetics to monitor daily blood sugar method used for infants
6 Components of Blood After centrifuging 55 % plasma 45 % cells 99 % RBCs < 1 % WBCs and platelets 19-6
7 Blood Plasma 0ver 90% water 7% plasma proteins made in the liver normally confined to bloodstream Albumin / solute vs solvent & osmosis maintains blood osmotic pressure Globulins (immunoglobulins) antibodies bind to foreign substances called antigens form antigen-antibody complexes Fibrinogen - produced by liver for blood clotting / liver disease > clotting problem 2% other substances electrolytes, nutrients, hormones, gases, waste products
8 Formed Elements of Blood 1. Red blood cells (erythrocytes) 2. White blood cells (leukocytes) Granular leukocytes Neutrophils / Eosinophils / Basophils Agranular leukocytes Lymphocytes = Helper T cells, B cells (plasma cells produce antibodies), and Natural Killer T cells Monocytes becomes a macrophage when leaving the blood stream 3. Platelets - special cell fragments that help form clots
9 Hematocrit The percentage of total blood volume occupied by RBC s. Normal females = 38-46% Females loose RBC s during menstruation and have lower levels of testosterone. Normal males 40-54% Testosterone stimulates the synthesis of erythropoietin (EPO) by the kidneys that stimulated RBC production in the red bone marrow.
10 Anemia is a drop in hematocrit. There are many different types of anemia caused by many different conditions. Polycythemia is a high hematocrit 65% or higher. Increases blood viscosity from abnormal production of RBC s, tissue hypoxia, dehydration and blood doping or the use of EPO by athletes.
11 Formation of Blood Cells Most blood cells types need to be continually replaced die within hours, days or weeks RBCs = negative feedback WBCs = response to pathogens or foreign antigens Process of blood cells formation is Hematopoiesis or Hemopoiesis In the embryo Hematopoiesis occurs in yolk sac, liver, spleen, thymus, lymph nodes & red bone marrow In adult occurs only in red marrow of flat bones like sternum, ribs, skull & pelvis and ends of long bones (femur etc.)
12 Disappears by about 12 weeks
13 Granular leukocytes eosinophils neutrophils basophils STEM CELLS (in bone marrow In adults) Immature macrophagas (monocytes) Agranular leukocytes mature macrophagas B lymphocytes T lymphocytes megakaryocytes Monocytes leave the blood Stream to become Macrophages platelets
14 Hematopoiesis Resides in bone marrow 99% of Formed elements 0.1% of Formed elements
15 Hemopoietic Growth Factors Regulate differentiation & proliferation Erythropoietin (EPO) - Oxygen dependent produced by the kidneys (90%) & liver (10%) / It increases RBC precursors (cells that will become RBC s) Thrombopoietin (TPO) hormone from liver stimulates platelet formation Cytokines are local hormones of bone marrow produced by some marrow cells to stimulate proliferation in other marrow cells colony-stimulating factor (CSF) & interleukin stimulate WBC production
16 Red Blood Cells or Erythrocytes Contain oxygen-carrying protein Hemoglobin that gives blood its red color 1/3 of cell s weight is hemoglobin Biconcave disk increased surface area/volume ratio flexible shape for narrow passages no nucleus or other organelles no cell division or aerobic respiration Normal RBC count male 5.4 million / mm female 4.8 million / mm 3 new RBCs enter circulation at 2 million / second
17 RBC Life Cycle RBCs live only about 120 days (4 months) wear out from bending to fit through capillaries no repair possible due to lack of organelles Worn out cells removed by fixed macrophages in spleen & liver Breakdown products are recycled
18 Erythropoiesis: Production of RBCs Begins in the red bone marrow with a proerythroblast. These divide until they produce cells that start to produce hemoglobin Many steps later the nucleus is ejected & a reticulocyte is formed Nucleus ejection gives RBC its concave shape Retain some mitochondria, ribosomes and ER Reticulocytes escape from bone marrow into the blood through sinusoid capillaries & mature in 1-2 days. (Lose ER) Every hour, about 180 million newly formed red blood cells enter the bloodstream
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20 Normal Reticulocyte Count Should be.5 to 1.5% of the circulating RBC s Low count in an anemic person might indicate bone marrow problem leukemia, nutritional deficiency or failure of red bone marrow to respond to erythropoietin stimulation High count might indicate recent blood loss or successful iron therapy
21 Recycling of Hemoglobin Components In macrophages of liver (Kupffer cells) or spleen globin portion broken down into amino acids & recycled heme portion split into iron (Fe +3 ) and biliverdin (green pigment)
22 Hemoglobin ( Hgb ) million Hgb molecules per RBC 4 heme groups per Hgb molecule o Each heme contais Fe 2+ combines reversibly with 1 oxygen molecule Therefore each RBC carries 2 Billion atoms of oxygen Hgb level and the total number of RBC s indicate the O 2 carrying capacity of the blood
23 Transport of Oxygen and Carbon Dioxide Each gas is carried at a different site on the Hgb molecule so there is no competition The Hgb carries both CO 2 and O 2. The O 2 is attached to Fe 2+ of the heme and the CO 2 attaches to amino acids within the globin part of Hgb Hgb transports 23% of total CO 2 waste and 99% of O 2 Hgb + O 2 is Oxyhemoblobin & is bright red Hgb w/out O 2 is Deoxyhemoglobin & is blueish
24 Feedback Control of RBC Production Tissue hypoxia (cells not getting enough O 2 ) high altitude / lower O 2 pressure anemia- RBC production falls below RBC destruction circulatory problems, emphysema, lung disease Kidney & liver response to hypoxia release erythropoietin speeds up development of proerythroblasts into reticulocytes 19-24
25 Anemia Not enough functional RBC s or a reduction in their Hgb content oxygen-carrying capacity of blood is reduced fatigue, cold intolerance & paleness lack of O 2 for ATP & heat production Types of anemia 1. iron-deficiency =lack of absorption or loss of iron 2. pernicious = lack of intrinsic factor for B12 absorption. B12 needed for RBC production. 3. hemorrhagic = loss of RBCs due to bleeding (ulcer) 4. hemolytic = RBC burst open 5. thalassemia = hereditary deficiency of hemoglobin 6. aplastic = destruction of bone marrow (radiation / toxins / antibiotics)
26 Sickle-cell Disease Genetic defect in hemoglobin molecule (Hb-S) that changes 1 amino acid (puts a valine where gluatamic acid should be) at very low O 2 levels, RBC is deformed by changes in hemoglobin molecule within the RBC sickle-shaped cells rupture easily = causing anemia & clots Found among populations in malaria belt Mediterranean Europe, sub-saharan Africa & Asia Person with only one sickle cell gene increased resistance to malaria because RBC membranes leak K + & lowered levels of K + kill the parasite infecting the red blood cells
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29 Blood Groups and Blood Types Antibodies are In the Plasma RBC surfaces are marked by genetically determined glycoproteins & glycolipids called antigens distinguishes at least 24 different blood groups ABO, Rh, Lewis, Kell, Kidd and Duffy systems
30 ABO Blood Groups Antigen - something that can cause an immune response Based on 2 glycolipid antigens called A and B found on the surface of RBCs display only antigen A -- blood type A display only antigen B -- blood type B display both antigens A & B -- blood type AB display neither antigen -- blood type O Plasma contains antibodies to the A or B antigens on the RBC s Anti - A antibody reacts with antigen A Anti - B antibody reacts with antigen B Remember-the antibody is in the serum/ pack cell vs whole blood
31 RH Blood Groups The antigen discovered in blood of Rhesus monkey People with Rh antigen on RBC surface are Rh+. Normal plasma contains no anti-rh antibodies Different from ABO blood groups - Antibodies are already in plasma Antibodies develop to Rh+ blood only by a Rh- person & only after exposure to the Rh antigen (blood) - this is different from ABO antibodies Anti-Rh antibodies only produced after 1 st exposure of a Rh- person to Rh+ blood during transfusion
32 Universal Donors and Recipients People with type AB blood called Universal Recipients since have no antibodies in plasma can only receive pack cells / Type O whole blood has antibodies against Type A & B & Type AB & Type A & type B whole blood have antibodies against the other type in their serum also People with type O blood cells called Universal Donors since have no antigens on their cells can only donate pack cells / their serum still has antibodies to Type A or Type B or Type AB
33 Transfusion and Transfusion Reactions Transfer of whole blood, cells or plasma into the bloodstream of recipient used to treat anemia or severe blood loss Incompatible blood transfusions antigen-antibody complexes form between plasma antibodies & foreign proteins on donated RBC's causes agglutination clumping donated RBCs become leaky & burst (hemolysis) loose hemoglobin / causes kidney damage / jaundice
34 Blood Transfusions When blood is removed from someone it can be stored several ways before it is given by IV (intravenous) to a person as a transfusion. 1. If the blood is stored without doing anything to it, then it is "whole blood". This unit of blood would consist of the blood cells (WBC s, RBC s & platelets) and the liquid part called the plasma
35 2. Some times the unit of blood will be centrifuged. This spinning causes the heavy cells (RBC's & WBC's) to go to the bottom of the bag. The liquid part (plasma) is poured off leaving only the cells in the bag. This unit is called pack cells. There is no serum (plasma) in the bag. Pack cells then have no serum and therefore have no antibodies. This is important because the antibody against the other types of blood is in the serum. A whole blood unit of type O would normally have both anti A & anti B in the serum. A pack cell unit of type "O" blood would only have the O type cells and no anti A or anti B antibodies. This pack cell unit could be given to any body since there are not any antibodies to A or B or AB blood. The O type cells do not have any antigens on the surface of the RBC that would cause a reaction to an A, B, or AB whole blood person that would receive this blood.
36 3. Some times the serum is stored and that is all that is transfused. People with hemophilia get this type of transfusion because they need the clotting factors that are in the serum.
37 Hemolytic Disease of the Newborn (HDN) (Erythroblastosis Fetalis) 1. Rh neg. mom with Rh + baby 2. Cells from Rh+ baby enter mother s blood stream at birth 3. Mother sensitized / antibodies form to fight Rh+ blood of 2nd Rh+ pregnancy causing hemolysis (HDN) of RBC RhoGam binds to fetal blood cells preventing mother from making antibodies against the baby s blood
38 Platelet (Thrombocyte) Anatomy Disc-shaped, 2-4 micron cell fragment with no nucleus / limited life span Normal platelet count is 150, ,000mm 3
39 Hematopoiesis of Platelets Resides in bone marrow 99% of Formed elements 0.1% of Formed elements
40 Platelets Life History Platelets form in bone marrow Myeloid stem cell form Megakaryocyte whose fragments form Platelets Short life span (5 to 9 days in bloodstream) formed in bone marrow few days in circulating blood aged ones removed by fixed macrophages in liver and spleen trauma can deplete platelets leading to bleeding problems several days late
41 Hemostasis Stoppage of bleeding in a quick & localized fashion when blood vessels are damaged Prevents hemorrhage (loss of a large amount of blood) 3 ways to stop bleeding 1. Vascular spasm 2. Platelet plug formation 3. Blood clotting (coagulation = formation of fibrin threads)
42 1. Vascular Spasm Damage to blood vessel stimulates pain receptors Reflex contraction of smooth muscle of small blood vessels in the area of wound Can reduce blood loss for several hours until other mechanisms can take over Only for small blood vessel or arteriole
43 2. Platelet Plug Formation Circulating platelets become sticky when exposed to collagen called platelet adhesion leading to platelet aggregation Platelet plug formation along with vascular spasm may stop bleeding if the hole is small enough.
44 Platelet Adhesion Platelets stick to exposed collagen underlying damaged endothelial cells in vessel wall
45 Platelet Aggregation Activated platelets stick together and activate new platelets to form a mass called a platelet plug Plug may be reinforced by fibrin threads formed during clotting process if necessary
46 3. Blood Clotting Blood drawn from the body thickens into a gel gel separates into liquid (serum) and a clot of insoluble fibers form (fibrin) in which the cells are trapped Clotting is a cascade of reactions in which each clotting factor activates the next in a fixed sequence resulting in the formation of fibrin threads (clot) Intrinsic Pathway activated by trauma inside the vascular system. Quicker Extrinsic Pathway begins with damage to a blood vessel or surrounding tissue that causes blood to escape the vascular system. Slower
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48 Thrombosis vs. Embolism Thrombosis clot (thrombus) forming in an unbroken blood vessel forms on rough inner lining of BV or valve of heart forms if blood flows too slowly (stasis) allowing clotting factors to build up locally causing coagulation may dissolve spontaneously or dislodge & move Embolus - a moving obstruction /a moving thrombus clot, air bubble or fat from broken bone in the blood ex. pulmonary embolus is a clot found in lungs that usually originates in leg primary cause of strokes (blockage of brain blood vessels) and myocardial infarctions (blockage of the coronary arteries)
49 Anticoagulants and Thrombolytic Agents Anticoagulants suppress or prevent blood clotting; heparin administered during hemodialysis and surgery warfarin (Coumadin) antagonist to vitamin K so blocks synthesis of clotting factors slower than heparin stored blood in blood banks treated with citrate phosphate dextrose (CPD) that removes Ca 2+
50 Hemophilia Inherited deficiency of clotting factors bleeding spontaneously or after minor trauma subcutaneous & intramuscular hemorrhaging nosebleeds, blood in urine, articular bleeding & pain Treatment is transfusions of fresh plasma or concentrates of the missing clotting factor
51 WBC Anatomy and Types All WBCs (leukocytes) have a nucleus and no hemoglobin All have jobs in the immune system Granular or Agranular classification based on presence of cytoplasmic granules made visible by staining Granulocytes: (also called polymorphonuclear cells ) Neutrophils Eosinophils Basophils Agranulocytes: Monocytes Lymphocytes
52 Immunity Innate Immunity also called non-specific immunity Respond without specificity Monocytes, Neutrophils, Basophils, Eosinophils Adaptive Immunity specific immunity Respond to specific invaders using recognition molecules Lymphocytes
53 Hematopoiesis of WBC S Resides in bone marrow
54 Neutrophil Function Fastest response of all WBC to bacterial invasion Direct actions ( fight ) against bacteria by: phagocytosis release lysozymes which destroy / digest bacteria release defensin proteins that act like antibiotics & poke holes in bacterial cell walls destroying them release strong oxidants (bleach-like, strong chemicals ) that destroy bacteria Numbers increase with bacterial infection
55 Eosinophil Function Leave capillaries to enter tissue fluid Release histaminase slows down inflammation caused by basophils Attack parasitic worms Phagocytize antibody-antigen complexes
56 Basophil Function Involved in inflammatory and allergy reactions Release heparin, histamine & serotonin heighten the inflammatory response and account for hypersensitivity (allergic) reaction Increases permeability of capillaries Leading to a red, hot, swollen & painful area Numbers increase with allergic reaction
57 Lymphocytes develop into T or B Cells B cells destroy bacteria and their toxins turn into Plasma Cells that produces antibodies T cells become Helper T cells or Natural killer cells -Helper T cells help B cells develop into plasma cells -Natural killer cells a special type of T cell / attack viruses, fungi, transplanted organs, cancer cells & some bacteria directly / cell to cell killing action Numbers increase with viral infection
58 Monocyte Function Can be wandering or fixed Also called Phages Take longer to get to site of infection, but arrive in larger numbers Called a macrophage when it leaves the blood stream to the interstitial space or to the alveoli of the lung Destroys microbes and cleans up dead tissue following an infection Fixed - in lungs, spleen & liver (Kupffer cells) Numbers increase with bacterial infection
59 WBC Physiology Less numerous than RBCs - 0.1% of formed elements 5000 to 10,000 cells per mm 3 1 WBC for every 700 RBC Leukocytosis is a high white blood cell count microbes, strenuous exercise, anesthesia or surgery Leukopenia is low white blood cell count radiation, shock or chemotherapy Only 2% of total WBC population is in circulating blood at any given time rest is in lymphatic fluid, skin, lungs, lymph nodes & spleen
60 Emigration / Phagocytosis / Chemotaxis WBCs roll along endothelium, stick to it & squeeze between cells. adhesion molecules (selectins) help WBCs stick to endothelium displayed near site of injury Other adhesion molecules (integrins) found on neutrophils assist in movement through wall Chemotaxis stimulated by kinins (from tissue damage) & toxins from bacteria / The macrophages & neutrophils leave the vessel to the interstitial space Pus: WBC, bacteria, dead cells, tissue fluid
61 Leukemia Acute Leukemia uncontrolled production of immature leukocytes crowding out of normal red bone marrow cells by production of immature WBC / not effective in fighting infection even with increased numbers / rampant inf. prevents production of RBC & Platelets Chronic Leukemia accumulation of mature WBC in bloodstream because they do not die classified by type of WBC that is predominant--- ex. monocytic, lymphocytic.
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