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The Cardiovascular System

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Presentation on theme: "The Cardiovascular System"— Presentation transcript:

1 The Cardiovascular System
Overall function: transport nutrients, gases, hormones, wastes, immune cells, etc. throughout the body It has 3 main parts: Fluid = blood (Ch. 19), which is a fluid connective tissue A pump = the heart (Ch. 20) Pipes/tubes/hoses = blood vessels (Ch. 21) Fig. 20-1, p. 670

2 Ch. 19 – Blood = a specialized fluid CT containing cells that are suspended in a fluid matrix Blood keeps you happy!

3 Functions of blood 1. Transportation of:
Dissolved gases, nutrients, hormones, metabolic wastes, heat, etc. 2. Regulation of the pH and ion composition of interstitial fluid Blood contains buffers to stabilize pH The constant diffusion between blood and interstitial fluid eliminates ion concentration differences between them 3. Restriction of fluid loss at injury sites Due to hemostasis and clotting 4. Defense against toxins and pathogens By white blood cells and antibodies 5. Body temperature stabilization Blood can absorb, redistribute, and/or dissipate heat

4 Characteristics of normal whole blood
1. Temperature ~ 38°C (100.4°F) 2. Viscosity = stickiness, cohesiveness, or thickness Blood is 5X more viscous than water When viscosity ↑ even more (e.g. during dehydration), → ↑ resistance to flow, so it’s harder for the heart to pump 3. pH = (slightly alkaline) 4. Blood volume Can be estimated (in liters) as ~ 7% of body weight (in kg) Adult male: 5-6 liters Adult female: 4-5 liters

5 The composition of whole blood
1. Plasma (~ 55%) = a fluid matrix 2. Formed elements (~ 45%) = blood cells and cell fragments Red blood cells (RBCs, or erythrocytes) White blood cells (WBCs, or leukocytes) Platelets (“thrombocytes”) Hemopoiesis = blood cell formation Hemocytoblasts in the bone marrow differentiate → myeloid stem cells + lymphoid stem cells Lymphoid stem cells differentiate → lymphocytes Myeloid stem cells differentiate → other formed elements Fig. 19-1, p. 640

6 Plasma Is similar in composition to interstitial fluid, except plasma has many more proteins Fig. 19-1, p

7 Formed elements See Table 19-3 for more details Fig. 19-1, p

8 Red blood cells Are a.k.a. RBCs, or erythrocytes
Make up 99.9% of formed elements There are ~ 4-6 million RBCs per μL (mm3) of whole blood Are packed full of hemoglobin = a red-pigmented protein which carries most (~ 98.5%) of the O2 in blood, and some CO2 too Hematocrit = the % of whole blood that is formed elements It’s a.k.a. the packed cell volume (PCV) Average in males = 46% Average in females = 42% The sexes are different because androgens stimulate erythropoiesis Fig. 19-2a, p. 644 + Platelets

9 RBC structure RBCs are biconcave discs about 8 μm in diameter
In mammals, RBCs do not contain a nucleus or most other organelles when mature They retain the cytoskeleton They do not have mitochondria No nucleus means they cannot divide, so they have a limited lifespan (~ 120 days) That’s OK: ~ 3 million new RBCs are produced per second in the red bone marrow Fig. 19-2bc, p. 644

10 Advantages of a biconcave disc shape
1. A large surface area-to-volume ratio, which… ↑ Diffusional exchange across the RBC membrane 2. It facilitates flow through narrow vessels RBCs stack single-file like dinner plates 3. It allows bending and flexing of the RBC membrane RBCs can flow through 4 μm diameter vessels! Fig. 19-2d, p. 644

11 Hemoglobin (Hb) = globin (4 polypeptides) + 4 heme units
The polypeptides (in adults) = 2 α and 2 β chains Heme = an iron-containing pigment (which is bright red when O2 is bound to it) O2 reversibly binds to the iron (Fe2+) in the heme Each Hb molecule can therefore bind to and carry 4 O2 Hb (hemoglobin or deoxyhemoglobin) + O2 ↔ HbO2 (oxyhemoglobin) Note: the globin of Hb can bind to and transport CO2 during low-O2 conditions (forming carbaminohemoglobin) Normal Hb range (in whole blood) = 12-18 g/dL Fig. 19-3, p. 645

12 RBC formation and turnover
Fig. 19-5, p. 647 RBC formation and turnover (from globin)

13 Erythropoiesis = RBC production
Hemocytoblast Myeloid stem cell (begin making Hb) Erythropoiesis = RBC production Reticulocytes: • Make up < 1% of circulating RBCs • Mature after about a day in the blood Fig. 19-6, p. 648

14 More on erythropoiesis
It requires: Amino acids (for the globin of Hb) Iron (for the heme of Hb) Vitamins (B12, B6, and folic acid), which are necessary cofactors Intrinsic factor from the stomach (to absorb B12 from dietary sources) The stimulus for RBC production is hypoxia = low tissue O2 Some causes of tissue hypoxia: Anemia (= ↓ O2-carrying capacity of the blood) This is often caused by a decreased hematocrit or [functional Hb] Low blood flow to the kidneys Decreased O2 content of the air (e.g. high altitude) Lung damage Hypoxia causes erythropoietin (EPO) to be released from the kidneys EPO stimulates erythropoiesis, by: 1. Stimulating mitosis in erythroblasts and their associated stem cells 2. Increasing RBC maturation and Hb synthesis rate EPO can increase RBC production 10X (up to 30 million/sec!!!)

15 Blood types Antigens = substances (usually proteins) that can trigger an immune response Surface antigens are found on cell membranes; they’re “ID tags” that are recognized by immune cells as being either from you (“self” or “normal”) or not from you (“non-self” or “foreign”) Antibodies (immunoglobulins) = plasma proteins that can recognize and bind to specific antigens RBC membranes may have glycolipid or glycoprotein surface antigens (specifically called agglutinogens) The most important agglutinogens = A, B, and Rh; which ones are present is genetically determined The plasma may contain certain anti-RBC antibodies (specifically called agglutinins) E.g. anti-A and anti-B (their presence is also genetically determined); anti-Rh (previous exposure to Rh is needed for it to be present) The binding of antibodies to antigens can cause: Agglutination (clumping) – causing downstream tissue to die; and/or Hemolysis (rupture of RBCs) – causing vasoconstriction, shock, and kidney damage Fig. 19-7b, p. 651

16 ABO blood types and transfusions
When figuring out if a particular blood transfusion will be theoretically successful (i.e., the recipient won’t have a potentially lethal cross-reaction), ask yourself: “Does the recipient’s blood contain antibodies that can attack antigens on the donated red blood cells?” Yes? – Very BAD  No? – Probably O.K.  Fig. 19-7a, p. 651

17 The Rh factor “Rh” comes from the Rhesus monkey, in which this antigen was first studied They’re also called D antigens A person with Rh antigens on their RBCs is Rh+ (Rh positive) A person without Rh antigens on their RBCs is Rh- (Rh negative) Major differences compared to A and B antigens: An Rh- person who has never been exposed to Rh+ blood does NOT have anti-Rh antibodies Anti-Rh antibodies from a mother can cross the placenta and enter the fetal bloodstream This can cause hemolytic disease of the newborn (HDN), a.k.a. erythroblastosis fetalis – see the next slide

18 Rh factor and pregnancy
Fig. 19-9, p

19 Blood type testing (Anti-Rh) In a lab, the blood sample is mixed with various antibodies Cross-reaction (clumping) indicates the presence of the cor-responding antigen Fig. 19-8, p. 652

20 White blood cells Are a.k.a. WBCs, or leukocytes
Make up < .1% of formed elements ( ,000/μL) Are nucleated Do not have hemoglobin Circulate in the blood for a limited time They migrate to connective and lymphoid tissues in the body So circulating WBCs are only a fraction of the total WBCs in the body General function: defense against pathogens, toxins, and abnormal cells (more on this in Chapter 22) Traditional classification: Granulocytes (have stained vesicles): Neutrophils, eosinophils, and basophils Agranulocytes (apparently lack vesicles after staining): Monocytes and lymphocytes

21 Characteristics of circulating WBCs
1. They can migrate out of the bloodstream First, they adhere to the wall of a blood vessel (margination) Then, they squeeze between the endothelial cells of the vessel wall to escape into the tissues (emigration or diapedesis) 2. Amoeboid movement They can move along vessel walls and throughout the tissues 3. Positive chemotaxis They are attracted to specific chemical stimuli 4. Phagocytosis (= engulfing pathogens, cell debris, etc.) Microphages = neutrophils and eosinophils Macrophages = monocytes

22 Neutrophils Are a.k.a. polymorphonuclear leukocytes
Normally are the most numerous WBC (50-70%) Are highly mobile, but have a relatively short lifespan Structure: They contain relatively neutral-staining granules (i.e. not very pink or very purple) They are ~ 12 μm in diameter They have a multi-lobed nucleus Functions – the “first line of defense”: 1. Phagocytize pathogens (usually bacteria): Especially those “marked” by antibodies or complement proteins 2. Destroy pathogens by using: Strong oxidants (e.g. H2O2) Defensins = chemicals that poke holes in bacterial membranes Digestive enzymes (e.g. lysozyme) 3. Release signaling chemicals, such as: Prostaglandins (which promote inflammation) Leukotrienes (which attract other WBCs) Fig a, p. 656

23 Eosinophils Normally make up 2-4% of WBCs Structure: Functions:
They contain pink-, red-, or orange-staining granules They usually have a bi-lobed nucleus They are ~ 12 μm in diameter Functions: 1. Via exocytosis, release toxic compounds (e.g. nitric oxide) onto large pathogens (such as some parasitic worms) 2. Phagocytize antigen-antibody complexes 3. Release antihistamine Which inhibits the inflammatory response, limiting the spread of inflammation to adjacent tissues Fig b, p. 656

24 Basophils Are normally rare: they make up < 1% of WBCs Structure:
They contain purple-staining granules They often have an obscure (purple) nucleus They are 8-10 μm in diameter Function – intensify inflammation: Release histamine, which dilates small vessels and increases capillary wall permeability (→ edema/swelling) Release heparin (an anti-coagulant) Fig c, p. 656

25 Monocytes Normally make up 2-8% of WBCs Structure: Functions:
They are agranular They are LARGE cells ( μm in diameter) (In lab, look for a cell 2-3X larger than a RBC) They have a kidney- or U-shaped nucleus Functions: Migrate to tissues; they may become wandering or fixed macrophages Aggressive phagocytosis Act as antigen-presenting cells for other WBCs Release chemotactic chemicals, which call other WBCs to the site of the battle Fig d, p. 656

26 Lymphocytes Make up 20-30% of the WBCs in the blood Structure:
They have a roundish nucleus, with a sliver of cytoplasm visible (no distinctive granules) They are 6-14 μm in diameter Frequently migrate between the blood and peripheral tissues At any given time, most are in the tissues and lymphoid organs Functions: 1. B cells are responsible for “humoral/ antibody-mediated immunity” They mature in the bone marrow, and migrate to the lymph nodes When activated, they differentiate into plasma cells, which secrete antibodies 2. T cells are responsible for “cell-mediated immunity” They mature in the thymus They attack virus-infected and cancerous cells, and transplanted tissues They include cytotoxic T cells, helper T cells, and suppressor T cells 3. Natural killer (NK) cells perform “immune surveillance” They recognize a wide variety (i.e., they are nonspecific) of antigens that they can attack and kill, such as microbes and cancerous cells Lymphocytes Fig e, p. 656

27 WBC origins/ differentiation
when activated, lymphocytes release… This figure is for big picture ideas only – DO NOT memorize the whole thing! Fig , p. 659

28 Platelets Are sometimes a.k.a. “thrombocytes” (but they’re not really cells in humans—just cell fragments) There are K per μL of whole blood Structure: They are fragments of megakaryocytes They are about 1-4 μm in diameter They stain purple in lab They contain vesicles (but the vesicles are not really visible in lab) Production = thrombocytopoiesis This process is stimulated by thrombopoietin from the kidney, interleukin-6, and multi-CSF 1 megakaryocyte → ~ 4000 platelets “Live” (circulate) for about 9-12 days About 1/3 of the total amount in the body are stored in the spleen and other organs, ready to be mobilized if needed Functions: 1. Release clotting chemicals 2. Form a platelet plug (= a temporary patch over a hole in a blood vessel) 3. Contract after the clot has formed, which reduces the size of hole in the vessel Platelets Fig. 19-2a, p. 644

29 Hemostasis = the stoppage of bleeding Consists of 3 phases:
1. The vascular phase 2. The platelet phase 3. The coagulation phase (blood clotting) Fig , p. 663

30 1. The vascular phase A. Vascular spasm = a reflexive contraction of the smooth muscle in the wall of the blood vessel The vessel diameter ↓, blood flow ↓, so blood loss ↓ B. Endothelial changes: The endothelial cells contract, exposing the basement membrane to the blood The endothelial cells release chemicals and hormones, including endothelins, which: ↑ The smooth muscle contraction ↑ Endothelial cell division to accelerate repair The endothelial cell membranes become “sticky” So the vessel walls may stick together to repair small breaks (such as in capillaries), and it’s easier for platelets to attach Fig , p. 662

31 2. The platelet phase A. Platelet adhesion – platelets adhere to the sticky endothelium, and the exposed basement membrane and collagen B. Platelet aggregation → platelet plug formation C. Newly arriving platelets are activated and secrete chemicals (this is the 1st positive feedback loop): ADP → ↑ aggregation and secretion Thromboxane A2 and serotonin → vasoconstriction Clotting factors (see the next phase) Platelet-derived growth factor (PDGF) → vessel repair Ca2+ → ↑ aggregation and clotting Fig , p. 662

32 3. The coagulation phase (blood clotting)
Plasma contains clotting factors (procoagulants), which include Ca2+ and 11 different proteins (many of which are proenzymes) Activation (damage to a blood vessel wall) produces an enzyme cascade, ultimately leading to a blood clot (which traps blood and effectively seals the damaged area) There are 2 clotting pathways (both of which are activated upon damage): A. The extrinsic pathway (faster) – begins outside the bloodstream, in the vessel wall When endothelial cells or peripheral tissues are damaged, they release tissue factor (TF or Factor III) B. The intrinsic pathway (slower, but more fibrin is produced) – begins inside the bloodstream, with the activation of circulating proenzymes Proenzymes (usually Factor XII) are activated when they contact the exposed collagen fibers at the site of damage This pathway is assisted by the release of platelet factor (PF-3) from platelets Both the extrinsic and intrinsic pathways → activation of Factor X, which = the 1st step of the common pathway, ultimately leading to: Fibrinogen (soluble) → fibrin (an insoluble web) → a clot The coagulation phase starts ~ 30 seconds after the damage; hemostasis usually occurs within a few minutes if the damage is not too severe

33 3. The coagulation phase (blood clotting)
Fig , p. 663

34 More on blood clotting Control
Thrombin from the common pathway re-stimulates both the extrinsic (via TF) and intrinsic (via PF-3) pathways This is the 2nd positive feedback loop However, to keep clot formation from getting out of hand, at least 7 blood agents (enzymes, cofactors, and other chemicals) inhibit the process E.g. anticoagulant enzymes, heparin, prostacyclin, etc. Ca2+ and vitamin K are required for proper clotting All three pathways require Ca2+ Vitamin K is required for the synthesis of clotting factors by the liver Clot retraction and fibrinolysis After coagulation, the platelets contract → clot retraction As healing occurs, the clot is eventually dissolved (= fibrinolysis) by the enzyme plasmin (which is activated by plasminogen)

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