One Week of Notes March 1-3
One Week of Notes March 1-3 Biol 2230-001
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This 59 page Class Notes was uploaded by Madeline Notetaker on Thursday March 3, 2016. The Class Notes belongs to Biol 2230-001 at Clemson University taught by Dr. John Cummings in Spring 2016. Since its upload, it has received 20 views. For similar materials see Human Anatomy & Physiology II in Biological Sciences at Clemson University.
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Date Created: 03/03/16
L YMPHOCYTE PRODUCTION Produced by stem cells in red bone marrow T cells become immunocompetent in thymus Acquire receptors on surface to interact with specific antigens B cells become immunocompetent in bone marrow L YMPHOCYTE PRODUCTION Produced by stem cells in red bone marrow T cells become immunocompetent in thymus B cells become immunocompetent in bone marrow Immunocompetent cells mature in secondary lymphoid organs L YMPHOCYTE PRODUCTION Produced by stem cells in red bone marrow T cells become immunocompetent in thymus B cells become immunocompetent in bone marrow Immunocompetent cells mature in secondary lymphoid organs Not fully functional until bound with antigen ANTIGEN-PRESENTING CELLS Engulfs pathogen and presents its fragments as antigens Lymphocytes are in body but not active yet,become activated when they interact with antigen CELL-MEDIA TED IMMUNE REPSONSE ANTIGEN CHALLENGE First encounter between naïve immunocompetent lymphocyte and antigen naïve immunocompetent= one that is ready to interact with something but has not yet (become immunocompetent in primary lymph organ (thymus or bone marrow),proteins on surface are specific of cells to antigens) Antigen= anything with markers 2 pathways: 1. Humoral pathway (uses B cells) 2. Cell mediated pathway (usesT cells) PRIMAR Y HUMORAL RESPONSE (THE FIRST ENCOUNTER) Antigens bind with surface receptors on naïve immunocompetent B lymphocyte Antigens are free floating in fluid/ plasma B lymphocyte becomes active! Clonal selection occurs Copies of cell that has the markers needed for antigen are reproduced Most clones become plasma cells which produce antibodies Antibodies attach to antigens and mark for destruction Some clone cells become memory cells Wait for another infection in the future SECONDAR Y HUMORAL RESPONSE (EACH ADDITIONAL EXPOSURE ) Same mechanism as primary But First response takes about 7-10 days to reach Titer (concentration of antibodies) Immune response faster Much more rapid Immune response lasts longer Long longevity Immune response more effective Produces more antibodies SOURCES OF HUMORAL IMMUNITY Active Exposure to antigen (antigen activates B cells, which leads to antibodies) Passive Antibodies from a source other than us End up with them,but produces somewhere else Natural We had to be infected Ex:natural passive- mom’s antibodies are given to baby by breastfeeding or placenta Artificial Ex:Artificial passive- vaccine that injects antibodies Ex:artificial active- immunization that injects a dead own antibodiese your cells respond and produce ANTIBOD Y STRUCTURE Complex proteins Called immunoglobulins 4 subunits: Heavy chains 2 identical ones Light chains 2 identical ones Variable region The area that contains light chains Have antigen binding sites Determine what antigen it will bind to Constant region Area that contains the heavy chains Dictates how something will be destroyed Antigen-binding site CLASSES OFANTIBODIES *Most are monomers=single units IgD The receptor on the surface of the B lymphocytes IgG Most abundant of all antibodies Main antibody present in late primary response and secondary response Longer lag to production Can cross placenta Bind and activate complement proteins IgE Typically not that many Increase in people who have allergies Can bind to mast cells,which produce histamine CLASSES OFANTIBODIES IgD IgG IgE IgA When two monomers are put together 4 receptor sites Accumulate in mucus and other bodily secretions Bind to antigens to prevent them from attaching to epithelial cells CLASSES OFANTIBODIES IgD IgG IgE IgA IgM 5 monomers attached 10 receptor sites First antibody secreted by plasma cells during primary immune response Diagnostic tool because can show if person had a recent infection Fix and activate complement Promote agglutination:antigens clump together causing other cells to flood to area ANTIBOD Y FUNCTIONS Formation of antigen-antibody complex Marking things! Provide site for binding of complement proteins At the constant region;once attached secrete perforins for lysing Block sites on pathogens So they cant bind with any other cells Called“neutralization” Cause clumping of antigen-containing cells To allow greater phagocytosis efficiency Cause clumping of soluble antigen molecules Precipitate them out of solution MONOCLONALANTIBODIES Commercially produced antibodies called“monoclonal antibodies” Infect another organism like horse, they produce antibodies,collect them and use for treatment, research… CELL-MEDIA TED IMMUNE RESPONSE Naïve immunocompetent T cell binds with antigen infected body cell Co-stimulatory signals are present Second binding also occurs T cell is activated occur) both of those things Clones are produced Clonal selection memory cellsbecome T CELLS All T cells have glycoprotein surface markers that are attachment points for different antigens • CD4 cells often called T4 cells, or helper T cells • CD8 cells also called T8 cells ** difference is what they attach to!! T CELLACTIVA TORS Class I MHC protein- linked antigens Endogenous= produced by body All body cells are capable of cellscing MHC except red blood Ex:cancer,viral cells CD8 cells bind to it Class II MHC protein- linked antigens Exogenous=antigen part comes from foreign antigen Ex:phagocytic cells that engulf bacterium CD4 cells bind to it ANTIGEN BINDING T cell antigen receptors bind to antigen-MHC complex This alone doesn’t activateT cell CO-STIMULA TORS T cell binding to other receptors onAPC, cytokines,interleukins Each promotes a different response Either facilitates or disables activation CELL-MEDIA TED IMMUNE RESPONSE T cell binds with antigen infected body cell Co-stimulatory signals are present T cell is activated Clones are produced Some clones become memory cells TYPES OF T CELLS CytotoxicT cells CD8 cells Directly attacks and kills cells with class I MHC Will lyse and break cell up to destroy it TYPES OF T CELLS HelperT cells A type of regulatory cell Regulate activity of other cells CD4 cells binds to cell with class II MHC and is activatedà activates CD8 cells and B cells TYPES OF T CELLS SuppressorT cells Shuts off clonal selection à stops immune response Cytokines or lysis chemicals (chemicals that activateT cells or that are sued to kill infected cells) activate suppressorT cells PRIMAR Y IMMUNE RESPONSE SUMMAR Y Need to know picture IMMUNE DISORDERS 3 groups: 1. Immunodeficiencies:any condition that causes immune cells to behave abnormally (could be insufficient production or have enough but not working properly) 2. Autoimmune diseases:when immune system attacks own body cells, lose ability to differentiate between self and antigens 3. Hypersensitivities:immune system responds to things that normally aren't antigenic;when harmless cells activate immune responses (allergens) IMMUNODEFICIENCIES 2 types: 1. Congenital= genetic, from birth 2. Acquired Severe combined immunodeficiency syndrome (SCIDS) Genetic disorder that fails to produce enoughT cells and also some enzymes that produce toxins IMMUNODEFICIENCIES Acquired immunodeficiencies (AIDS) Acquired from HIV virus that destroys helperT cells A subsequent infection kills that person AUTOIMMUNE DISEASES Multiple sclerosis (MS) Destroys white matter in the brainà lose conductivity AUTOIMMUNE DISEASES Multiple sclerosis Myasthenia gravis Immune cells attack any neuromuscular junction in skeletal muscle AUTOIMMUNE DISEASES Multiple sclerosis Myasthenia gravis Graves’ disease Immune system attacks thyroid gland Symptom is bulging eyes AUTOIMMUNE DISEASES Multiple sclerosis Myasthenia gravis Graves’ disease Juvenile diabetes Attack pancreatic cells that produce insulin AUTOIMMUNE DISEASES Multiple sclerosis Myasthenia gravis Graves’ disease Juvenile diabetes Lupus Attacks kidneys,heart, and lungs Associated with skin lesions/butterfly rash AUTOIMMUNE DISEASES Multiple sclerosis Myasthenia gravis Graves’ disease Juvenile diabetes Lupus Rheumatoid arthritis Attacks synovial membranes of joints HYPERSENSITIVITIES Immediate/acute Ex:allergic to bee stings Causes anaphylaxis Systemic release of histamine which causes systemic vasodilationà drop in blood pressure that can be fatal Most severe Response occurs in seconds HYPERSENSITIVITIES Subacute Response takes a couple of hours before we see it Ex:Transfusion reaction of blood HYPERSENSITIVITIES Delayed Response takes 1-3 days Ex:Poison ivy reaction TRANSPLANTS If you get something that’s not own cell, body will attack. Autograft= transplant from one part of body to another (SAME PERSON) Isograft= transplant from identical twin, identical MHC allograft= transplant from someone different, look for closely related, potential rejection Xenograft= transplant from different species (ex: pig heart valves) Involves supplying oxygen and elimination carbon dioxide; Closely linked to cellular respiration RESPIRA TOR Y SYSTEM COMPONENTS OF RESPIRA TION Pulmonary respiration of bodyt of air into and out External respiration Exchange between capillaries and lung space Gaseous transport Delivery of gas to tissues Circulation Internal respiration Exchange between blood capillaries and tissues of body A circulatory function RESPIRA TOR YAPPARA TUS Pathway that air has to follow: Air moves in usually through nose (a second way is through mouth), trachea splits to each lung (bronchi= the split), split into secondary bronchi, tertiary bronchi, bronchioles, terminal bronchioles, respiratory bronchioles (microscopic), alveoli * Sites of exchange 1. Conducting zone • Everything that is before the respiratory bronchioles • Moving air • Air gets cleansed, pull pathogens, pollen, dust out, also humidifies/moistens air, and also warms air 2. Respiratory zone • Where gas exchange occurs between lungs and capillaries NOSE= NORMAL ENTR YWA Y Only external structure of respiratory system! Passageway Warms and moistens By mucosa Filters Hair collects big particulates Resonating chamber Buzzing in sinus gives voice a tonal quality Not a respiratory function Olfactory receptors Sensory receptors Not a respiratory function NASAL CAVITY External nares Openings to nose Vestibule Enlarged cavity Vibrissae Stiff hair that lines vestibule Internal nares Opening in back of nasal cavity Point of constriction to slow air Paranasal sinuses Hollowed portion of bones in skull Help to lighten weight NASAL MUCOSAE (A MUCUS MEMBRANE ) Olfactory mucosa Smell receptors Respiratory mucosa Pseudostratified ciliated columnar epithelium (PCCE) Goblet cells- secrete mucus Mucous glands- also secrete mucus Serous glands- secrete enzymes Defensins- secretions that function as natural antibiotics (kill bacteria) Cilia- beating to make motion toward throat to make us cough PHAR YNX =pathway that connects nasal and oral cavities to lower parts Nasopharynx Made of PCCE Uvula-At back of oral cavity,closes off nasal cavity when swallowing Pharyngotympanic tubes- regulates inner ear pressure Oropharynx Fauces- bend in oral cavity to give direction down Made of stratified squamous because food is rough Laryngopharynx Stratified squamous Flap closes when swallowing LAR YNX Made of rigid cartilage Entrance into trachea Provides open airway Directs food and air Produces voice Where the buzzing originates VOCAL STRUCTURES Vocal folds 2 sets of vocal folds that surround glottis Vibrate when air comes out Glottis the opening that epiglottis covers Vestibular folds Can change diameter of opening and tension Changes pitch of buzz TRACHEA Rigid tube from neck to mediastinum Made of C-shaped rings of hyaline cartilage Back of rings has smooth muscle Carina= the very last cartilage in trachea Forces a split into left and right lungs TRACHEAL LA YERS Cilia beat up toward throat to make us cough, 3 layers: mucosa, submucosa, adventitia BRONCHIAL 53&& Primary bronchi first branch Secondary bronchi 3 on right,2 on left Tertiary bronchi Carries air to segments of lobes Right lung has 10 segments Left has 8 or 9 Bronchioles Get smaller and smaller Terminal bronchioles Less than .5mm in diameter Respiratory bronchioles * Left lung has two lobes, right has three Microscopic LUNGS Pleural cavities Each lung is surrounded by sac Cardiac notch Allows heart to sit in Lobes Divided into segments Alveoli (alveolar sacs) AL VEOLAR STRUCTURE 1 cell layer thick! Type I cells Simple squamous epithelial Pulmonary capillaries Blood capillaries surrounding alveoli Respiratory membrane simple;only has to pass across two membranes (type I cells and pulmonary capillaries) Type II cells Cuboidal cells reduces water surface tension tohat allow gas to cross) Alveolar pores Want lungs to be at same pressure Connections between alveoli Alveolar macrophages Remove antigens in air PLEURAE Parietal pleura Serous membrane surrounding lungs Lines thoracic cavity Visceral pleura Immediate outside lining of lungs Pleural cavity Filled with fluid Between 2 layers Pleural fluids Makes lungs expand as chest expands PULMONAR YVENTILA TION Air follows a pressure gradient! Consists of: Inspiration= air moves into lungs Expiration= air pushed out of lungs Regulated by: Pressure Volume- regulates pressure Resistance- little bit of friction, negligible Surface tension- liquid resistance Compliance- stretchiness of lungs; more compliant= more change in volume PRESSURES Atmospheric- around us all the time 760 mmHg Intrapulmonary- pressure inside lungs that changes when we breathe When its below atmospheric,air moves in When its higher than atmospheric,air moves out Intrapleural- pressure in the pleural cavity Transpulmonary- difference between intrapulmonary and intrapleural BOYLE’S LAW Relationship between volume and pressure Remember:gas always expands to fill container P V = P V 1 1 2 2 if we expand,lower pressure If we compress,increase pressure BREA THING • A function of skeletal muscles: • Respiratory diaphragm pulls down when contracts to increase volume of thoracic cavity, at same time intercostal muscles contract to lift chestà decreases pressure so air moves in RESPIRA TOR YVOLUMES Tidal volume Normal amount of air moving in and out .5 liter Inspiratory reserve volume Excess volume we can pull in Little over 3 liters Expiratory reserve volume Excess amount we can force out Residual volume Air that stays in lungs Little over 1 liter Anatomical dead space Air in conducting zone that’s not contributing to gas exchange 15 mL Spirograph