Review sheet lymphatic and immunity reduced 2018-2 PDF

Title Review sheet lymphatic and immunity reduced 2018-2
Author Lauren Kwist
Course Anatomy and Physiology
Institution Indiana University
Pages 9
File Size 515.4 KB
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CHAPTER 21-THE LYMPHATIC SYSTEM (reduced version spring 2018) 

List the three major functions of the lymphatic system. o 1. Fluid recovery o 2. Protection from pathogens o 3. Lipid absorption from small intestines o A network of vessels that penetrate nearly every tissue of the body, & a collection of tissues/organs that produce immune cells. Fluid leaked from capillaries is picked up by lymphatic system to send back to circulation. Lymphocytes: protect us from disease causing organisms. Lymph nodes are helpful to prevent and clear infection before reaching blood stream. 

List the components of the lymphatic system. Define primary and secondary lymphatic tissues. o 1. Lymph  Colorless fluid, contains WBCs that bathes tissues & drains thru the lymphatic system  Similar to blood plasma, but low in protein. Similar to serum, plasma without proteins. Similar glucose, water and ions, o 2. Lymph vessels – transport lymph, Lymphatic drainage, & lymph nodes o 3. Lymphatic tissue  rich in lymphocytes o 4. Lymphatic organs  Lymph nodes, spleen, tonsils, adenoids & thymus o 5. Lymphatic cells  B & T cells



Edema: define, know the 3 main causes, and the specific causes of each main cause. o Edema: fluid retention in the cavities or tissues of the body o Causes: Elephantsis.  1. ^ Capillary filtration (^ capillary BP or permeability) leakier. One cause is poor venous return. Systemic and circulatory has to have the same venous return  Poor venous return o Congestive heart failure & pulmonary edema o Insufficient muscular activity lead to edema  Kidney failure (water retention, hypertension) drives more fluid out of capillaries  Histamine makes capillaries more permeable, more fluid leaves, drops blood pressure  2. Low capillary reabsorption  Hypoproteinemia o Cirrhosis, famine, burns, kidney disease reduce plasma proteins. o Plasma oncotic pressure is due especially to blood albumin. Low, blood proteins, can be caused by cirrhosis which is a liver disease which is where it is formed. Diet, burns, loose fluid through it which contains plasma proteins. Kidney disease: loose more fluid.  3. Obstructed lymphatic drainage



Know the harmful consequences of edema. o 1. Circulatory shock –  Excess fluid tissue in spaces causes low blood volume & low BP, causing shock o 2. Tissue necrosis –  O2 delivery & waste removal are impaired o 3. Pulmonary edema & suffocation Dangerous o 4. Cerebral edema – Swelling in the brain, brain can’t get bigger because skull around it, uses 1

blood vessels and reduce blood flow to the brain. Lead to coma and death.  Headaches, nausea, seizures, & coma. Describe the basic anatomy of the lymphatic system: lymphatic capillaries, vessels, lymph nodes, and right lymphatic duct and thoracic duct emptying into the right and left subclavian veins. Capillaries blood, fluid leaks out and is picked up lymph, they’re closed at one end. They are one way, pick up fluid and drain it back towards the heart. Fluid enters, and proteins are pulled out, and sent back to the blood. Low pressure and they have valves. o Lymphatic capillaries converge to form collecting vessels. o They empty into lymph nodes. o Eventually collecting vessels converge to form lymphatic trunks & drain into major parts of their body. o Lymphatic trunks converge to form two collecting ducts, the largest of the lymphatic vessels:  The Right lymphatic duct is formed by the convergence of the right jugular, subclavian, & bronchomediastinal trunks in the RIGHT thoracic cavity. Receives lymphatic drainage from the right arm & R side of the thorax & heads & empties into the R subclavian vein.  The thoracic duct (on the L side) is larger & longer. Contains the prominent sac cisterna chyli that collects chyle (fatty intestinal lymph) that it collects after a meal. Then passes thru the diaphragm, & thorax where it receives additional lymph from L bronchomediastinum, subclavian, & jugular trunks & empties into L subclavian vein. This duct drains all of the body below the diaphragm & L upper limb & L side of the head, neck, & thorax.



Describe capillaries. the last o

o

o o

the uptake of fluid by lymphatic Relate to fluid loss by capillaries in chapter. Lymphatic system has no pump like the heart does, so lymph flows at at even lower pressure & speed than the venous return. Primary mechanism of flow:  Rhythmic contractions of lymphatic vessels:  Contract when the fluid stretches them. Valves of the lymphatic vessels prevent fluid from flowing backward. Lymph flow is also produced by skeletal muscles squeezing lymphatic vessels. Arterial pulsation – lymph vessels are often rapped with an artery. 2

Thoracic respiratory pump promotes lymph flow from abdominal to thoracic cavity as one inhales. o Rapidly flowing bloodstream draws lymph to sites. Lymphatic cells inclue natural kills cells, lymphocytes, and antigens presenting cells. o



Know the different categories of lymphatic cells: NK cells, B and T lymphocytes, antigen presenting cells. Know the roles of B and T lymphocytes and antigen presenting cells in immunity. o NK cells – natural killer cells  Large lymphocytes that attack & destroy bacteria, transplanted tissues, & host cells (cells of one’s own body) that have become infected.  Responsible for a mode of defense. o Lymphocytes:  T lymphocytes  Immunocompetent – capable of recognizing antigens presented to them by APCs.  Recognize, destroy, & attack foreign antigens  B lymphocytes  Immunocompetent  Make & secrete antibodies, bind to antigens o Antigen presenting cells (APCs)  Macrophages: found everywhere, wonder around in different places.  mobile APCs found in many places.  Phagocytize tissue debris, dead neutrophils, bacteria, foreign matter.  Dendritic cells:  mobile APCs of epidermis (Langerhans cells), mucous membranes & lymphatic organs.  Alters immune system to pathogens that have breached body surfaces.  Engulf foreign matter by endocytosis, migrate to nearby lymph node & activates immune reaction.  Reticular cells:  stationary APCs of lymphatic organs  contribute to connective tissue framework of lymphatic organs. 3



Define diffuse lymphatic tissues, primary and secondary lymphatic organs. o Diffuse lymphatic tissue:  Aggregations of lymphocytes in mucous membranes & connective tissues, rather than densely clustered.  Especially, mucosa-associated lymphatic tissue – respiratory, digestive, urinary, & reproductive tracts. Anywhere you have an opening to the outside. o Primary lymphatic organs:  Where T & B lymphocytes become immunocompetent (recognize & respond to antigens)  Red bone marrow – B lymphocytes  Thymus – T lymphocytes o Secondary lymphatic organs:  Lymph nodes, tonsils, spleen  Where immunocompetent cells migrate to after they mature in primary lymphatic organs. Sinusoids are specialized capillaries that fill the gaps in cells that do not have basement membranes. 

Know the roles of lymph nodes, thymus, spleen, tonsils. o Lymph nodes: basically, have lymph flowing in onside have lots of lymphocytes.  Most numerous lymphatic organs  Cleanses lymph & acts as a site of T & B cell activation. They multiply lymph nodes swell. o Thymus:  Activation of T lymphocytes  De-activation of self – recognizing lymphocytes o Spleen: large organ, it produces blood cells before you are born.  Produces blood cells in the fetus (& during severe anemia)  Role in immunity:  White pulp: contains lymphocytes & macrophages  Red pulp: RBCs leave & re-enter the capillaries of the spleen o Immune clearance of foreign antigens attached to RBCs. o Old RBCs are destroyed in the process; macrophages clear debris. o Tonsils:  Patches of lymphatic tissue located @ entrance of pharynx  Guard against inhaled & ingested pathogens  3 main sets:  1. Pharyngeal tonsil (adenoid)  2. Palatine tonsils o Largest & most often infected o Tonsillitis is inflammation of palatine tonsils  3. Lingual tonsils

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Define sinusoids of red bone marrow. o o o

Numerous small arteries enter nutrient foramina on bone surface & penetrate into the bone emptying in large sinusoids (open pore capillary) in the red bone marrow. Sinusoids drain into a central longitudinal vein that exits the bone the same route it entered in. Sinusoids are lined by endothelial cells.

Know the main types of pathogens and define and list the main types of infectious agents. o Pathogens: Things that make you sick  Infectious agents – Microbes that because disease Means that they can reproduce and be transmitted  viruses, bacteria, Protista, fungi, etc.  Toxins  Radiation 

Know the components of the first, second, and third lines of defense. o Nonspecific resistance  First line of defense:  External barriers Skin, lining of open tubes  Second line of defense:  Leukocytes & macrophages  Antimicrobial proteins  Inflammation  Fever o Specific defense Memory.  Third line of defense:  The immune system – T & B lymphocytes



Define and compare nonspecific resistance with specific defenses. o Nonspecific resistance: has a number of contributors, external barriers are between you and the outside world including skin. Lining of respiratory system. Mobilize defenses to the area. Vasoactive, vasodilatation of the capillaries of the area of the injury, increased blood flow to the area called hypoxemia, more leakier capillaries. Chemical signals recruit leukocytes. Chemotaxis, moving towards a chemical.  First 2 mechanisms (1st & 2nd line of defense)  They guard equally against a broad range of pathogens & their effectiveness does not depend on prior exposure – these defenses are present from birth. o Specific defense:  Immunity  Results from prior exposure to a pathogen & usually provides further protection only against that particular one.



List the components of nonspecific resistance. o External barriers: skin & mucous membranes o Phagocytic cells o Antimicrobial proteins o Inflammation o Fever 5



Mobilizing defenses – describe methods in inflammation. What are the roles of mast cells and basophils in releasing the vasoactive chemicals involved in mobilizing defenses? o Vasoactive chemicals from basophils, mast cells, & damaged tissues cause:  1. Hyperemia – increase blood flow to deliver leukocytes quicker  2. Increased capillary permeability  3. Recruitment of leukocytes via chemotaxis & colony stimulating factors.



Define hyperemia. o Increased blood flow



Describe the inflammatory response and the roles of hyperemia, increased capillary permeability, chemotaxis, and CSFs during inflammation. o Inflammatory response: mobilization of body’s defenses to injury & infection, containment & destruction of pathogens, & tissue repair & cleanup. o Local hyperemia:  Increase blood flow for more rapid delivery of leukocytes (also washes toxins & metabolic wastes from tissues)  Achieved by vasodilation. o Certain cells secrete vasoactive chemicals that dilate blood vessels: basophils & mast cells secrete histamine, cytokines.  Vasoactive chemicals also stimulate endothelial cells of blood capillaries & venules to contract slightly, widening the gaps between them increasing capillary permeability allowing easier movement of fluid. o One priority in inflammation is to prevent pathogens from spreading thru body.  Fibrin filters into tissue fluid in areas adjacent to the injury forming a sticky mesh that walls off & isolates bacteria & other microbes.  Heparin (anticoagulant) prevents clotting in the immediate are of injury so bacteria & pathogens are essentially trapped. o The chief enemies of bacteria are neutrophils which accumulate in inflamed tissue. o After emigrating from bloodstream, the exhibit chemotaxis-attraction to chemicals that guide them to the site of injury.  Neutrophils phagocytize & destroy bacteria.  Neutrophils also recruit macrophages & additional neutrophils by secreting cytokines called colony stimulating factors (CSFs act on stem cells), which stimulate leukopoiesis, more leukocytes and move to the site of injury. CSFs to red bone marrow stimulate leukopoiesis



What are the 4 cardinal signs of inflammation? Which of these signs are caused by hyperemia? o Redness - Due to hyperemia, blood flow increases to area. o Swelling - Edema due to increased fluid filtration from capillaries, more permeable. o Heat - Results from hyperemia, because of more blood flow. 6

o o o

Pain direct injury to nerves/pressure on nerves due to edema & stimulation of pain receptors. Inflammation appears to be an underlying contributor to many diseases.  Cardiovascular, Diabetes, Neurodegenerative disease Appears to be associated w/ metabolic disruption. Driven by diet, a lot of processed food, stimulates systemic inflammation throughout the body, correlated with obesity.



Describe the roles of neutrophils, mast cells, histamine, fibrin, chemotaxis, CSFs, etc. in the response to an infection and in an inflammation. o Neutrophils –  Accumulate in inflamed tissue & exhibit chemotaxis (attraction to chemicals such as bradykinins & leukotrienes)) to guide them to site of injury.  Phagocytize & destroy bacteria  Recruit macrophages & more neutrophils by secreting cytokines called CSFs which stimulate leukopoiesis. o Mast cells –  Mast cells & (basophils) secrete histamine & cytokine. o Histamine –  Dilates capillaries o Fibrin –  Clots, forming sticky mesh that blocks off & isolate bacteria to trap pathogens



What are NK cells and what do they do? o Natural killer cells o Large lymphocytes that attack & destroy bacteria, transplanted tissues, & host cells (cells of one’s own body) that have either become infected w/ viruses or cancerous. o Responsible for mode of defense called immune surveillance:  NK cells continually patrol the body “on the lookout” for pathogens or diseased host cells.



Describe the Macrophage system. o All of the body’s avidly phagocytic cells o Wandering cells that actively seek pathogens, o Reticular & other cells are fixed in place & phagocytize only the pathogens that go to them. o Widely distributed in connective tissues. o Specialized forms w/ specific localities.



Define and describe antigen presenting cells. Why are they critical for immunity? o Antigen-presenting cell o Required to activate immune response. o Help T cells recognize & attack foreign antigens b/c T cells sometimes cannot recognize such on their own.  Dendritic & reticular cells, B cells & macrophages.



Define immune clearance. Where does it occur? o Clearing foreign antigens from bloodstream, particularly of foreign antigens attaches to RBCs. o Spleen & liver

 

Define opsonization. Define the membrane attack complex.



Define pyrogen. 7

o o

Pyrogens are released causes reset to homeostatic level (negative feedback) Beneficial



Describe a fever Body has adjusted things to try to fight of an infection, temperature rising, but you’re still maintain a set point. o A protective response adjusting our body temperature. o If fever gets too high, you’re entering a very risky condition (103, 104) causing a positive feedback loop increasing metabolic rate increasing heat production & fever takes off uncontrollably. Doesn’t take much after 103 to start injuring nervous tissue/brain damage. o  The role of hypothalamus Where you set your body temperature. Pyrogens, chemicals that cause you to raise your temperature. Regulates body temperature, Pyrogens – endogenous made by neutrophils and macrophages makes – interleukin one, communication between leukocytes, and essentially make PGE & exogenous, PGE in the hypothalamus, esocanoids, causes a fever, by using NSAIDS. What are the beneficial and harmful effects of fever, why is a fever that is too high dangerous while lower fevers are beneficial? How do NSAIDS reduce fever? Aspirin and Ibuprofen, fever can be helpful promotes interfin, brings metabolic rate up. Higher temperature effects growth of bacteria and viruses. If your fever gets too high, between 103 and 104, etc. You have potential for a dangerous positive feedback loop. Increase metabolic rate, temperature, increase metabolic rate more and more, brain can’t handle high temperature, brain damage coma and death. Specific defenses: Relies on: List types of B and T cells, and their roles. T cells attack cells infected with pathogens, directly attack another cell. Memory T cells, helper T cells are required for an immune response. Go to the Thymus, then to lymphatic tissues and organs. B cells – antibodies are in the plasma called humeral immunity. Plasma cells, produce chemicals called antibodies, globulins, and gap memory cells which allow you to become immune. Define cell mediated and humoral immunity. Which lymphocyte type is responsible for each? Which type of immunity requires antibodies? T cells are cell mediated because they attack directly other cells, while B cells are humoral and are humoral immunity requires antibody. Describe the role of Macrophages and antigen presenting cells in immunity. MHC – major histocompatibility complex, What are MHC I and MHC II, what cells have each type, and what are their roles in the activation of T cells? All cells of body have MCH 1, MCH 2 are only on antigen presenting cells. What are the T and B cell receptors and their roles in activation of the cells? How does the activation of these cells involve MHC and antigen-presenting cells? What is the role of the helper T cell in this activation? -All cells have MHC1 giving trouble for organ transplants because MHC cells are different -MHC2 are found on antigen presenting cells. Antigens and antibodies: what are they, what do they do, where are they found? Antigens are found on cells, and antibodies are made by B cells. B cells make all different types, genetically distinct. Each one 8

produces a different antigen receptor. Antibody binds to antigen and destroys then. What mechanisms allow antibodies to inactivate antigens and destroy pathogens? Describe neutralization, agglutination, precipitation, opsonization, and activation of complement. How does each of these helps eliminate pathogens? Humoral Immunity, binding of antibodies to antigen inactivates the antigens by: Neutralization which is blocking viral binding sits and coating bacterial toxins, blocking site for virus to infect cell. Bind to toxins and cover It up, cannot interact anymore Agglutination of microbes. Precipitation of dissolved antigens, all enhances phagocytosis. Make it easier for macrophages to destroy an antigen. Activation of complement molecule which leads to cell lysis. When you have antibodies bound to a foreign, it activates compliment and makes a hole in the cell membrane. What are the roles of the antigen presenting cell, the MHC, the helper T cell, interleukins and cytokines, and B and T lymphocytes in immune responses? Helper T cells recognize the antigen on MCH and activates responses, B cells, to give us humoral immunity or production of antibodies and it activates T cells that attack by releasing chemical signals. -interleukins communicate between leukocytes & cytokines help activate T cells. Turn on immune responses, without these cells, immunity doesn’t work. -HIV knocks out helper T cells (selectively destroys) therefore we cannot make an immune response causing us to make it harder to fight off easy illnesses. Gets rid of helper T cells and makes AIDS.

Primary and secondary immune responses- define, describe, and compare. In first exposure to antigen X, your primary responses to antigen x is a low concentration of antibodies. During your second exposure to antigen X, you have a high concentration because of memory cells and you make them much quicker. If you’re supposed to a new antigen, you’ll get a ne...


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