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Content in the Lymphatic System
- lymph nodes
- diffuse lymphatic tissue and nodules
- lymphatic vessels
- spleen
- thymus
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Functions of the Lymphatic System
- filter dead material and infectious organisms from lymph fluid
- house germinating centers for lymphocytes
- vessels absorb fats from GI tract and return to the blood
- vessels return fluids in tissues not reabsorbed by capillaries to blood
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Structure of Lymphatic Vessels
- valves, thin walled and compliant
- start as tiny dead end vessels
- not tightly packed cell
- design of the system is not symmetrical; right side just shoulder and arm; left side does all the rest of body
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Lymph nodes
- have cortex and medulla
- -cortex contains germinating centers
- -medulla has reticular fibers for trapping and filtering items form lymph
- -WBC's hang out on fibers and phagocytize bacteria etc.
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Location of Nodes
axillary, cervical, and inguinal etc.
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Spleen structure
like a giant lymph node but functions are different (gets rid of old RBCs)
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Functions of the Spleen
- filters blood with reticular fibers
- connected to blood system
- stores about 1 liter of blood
- removes old RBC's from blood
- germinating centers for lymphocytes
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What is the thymus and where is it located?
- top of the heart
- it makes chemical/ hormones that stimulate WBC
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How does the lymphatic fluid return to the blood stream?
it goes to the subclavious vein and that dumps it in veins which return it to the heart
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Types of leukocytes
granular and agranular
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Types of granular leukocytes
- neutrophils
- basophils
- eosinophils
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Types of agranular leukocytes
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Neutrophil
- polymorphonucleated cells (PMN) (nucleus can take many shapes)
- phagocytosis (engolfs things)
- NSIS (non specific immune system)
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Basophil
- circulates in blood
- (closely related cell found in tissues; mast cell)
- allergic reactions
- Part of SIS (specific immune system)
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Eosinophil
- initate and suppress allergic reactions
- fight parasites and tapeworms
- part to SIS
- negitive feedback for basophils
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monocytes
- circulation precursors to marcophages
- take on many roles and specific names
- phagocytic cells
- function mainly with SIS
- they become antigen presenting cells (APC)
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lymphocytes
- B: make antibodies; part of AMI (antibody mediated immunity)
- T: fight infections through other means; part of CMI (cell mediated immunity)
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Natural killer cells
find cancer cells and virus infected cells on their own
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Non-specific resistance definition:
- innate mechanisms that all members of your species will have
- mechanism can not be enhanced with repeated exposure
- they system reacts the same to each infection; not specific response
- theres no memory component
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Non-specific resistance mechanisms of resistance:
- healthy skin
- mucous membrane
- tears, stomach acids, oils in skin
- phagocytic WBC's
- -create compoundsthat are cytolytic to pathogens as well as to surrounding tissue
- natural killer cells
- interferon
- complement system
- fever response
- inflammatory response
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Natural killer cells (NK)
- locate and destroy 'enemy' cells
- -dont need the help of other WBC's to find target and destroy it
- -first line of defense against cancer cells
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Interferon
- anti-viral warning compound; one of the cytokines
- -made by dying cells as a warning to healthy cells
- -uses that second messenger system
- -stimulates uninfected cells to make AVP (anti-viral proteins)
- -Can also activate NK cells
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Complement system
- set of plasma proteins made in liver
- activation or complement fixations leads to a series of enzymatic responses; cascade response
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Alternative Complement pathway
- complement protein C3 'spontaneously' splits due to the presense of certain ingredients in pathogentic, infected, & malignant cells
- or the plasma protein lectin blinds to bacterial components and casues C3 to split
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Antigen- antibody union
- classical pathway
- specific immunity
- leads to C3 activation
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Functions of the Complement system
- cytolysis of infectious organism (due to membrane attack complex)
- act as 'glue' for macrophages and the infectious target immunoadherence or opsonization
- causes enhancement of inflammatory response
- Clears Ag-Ab complexes by sticking them on RBC's and allowing macrophages to find and destroy the complexes as they pass through the liver or the spleen
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fever response
- release endogenous pyrogens
- alters action of the hypothalamus
- depress bacterial reproductions and viral replication
- promotes healing through increased metabolism
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inflammatory response
- redness, pain, swelling, and increased temp
- stop infection form spreading; bring in WBC's
- vasodilation allows things in blood to enter area
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Antigens
- anything "not of self"; foreign particles
- something's are highly immunogenic or antigenic
- -more elaborate compounds will have more antigenic regions
- antigenic determinants
- hapten: too small for system to 'see'
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Active acquired (specific) immunity
- active natural: get sick; survive; make Ab and become immune
- active artifical: get vaccine; make Ab's; ready if ever exposed
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Passive acquired immunity
- passive natural: mother to fetus
- passive artificial: borrow antibodies for short term immunity; can't wait for your own system to take the time to respond
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Antibodies:
define
proteins made specifically to bind to a specific antigen; lock and key mechanism
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Structure of antibodies
- constant region
- variable region
- Fc region: very end of the constant sem region
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Function of Ab's
- trap: agglutinate and precipitate the Ag's
- neutralization
- activate complement
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IgG
- make up ~ 80% of the serum antibodies
- half-life of 7-23 days
- a monomer
- activate the classical complement pathway
- Fc portion can bind to macrophages and neutrophils
- is able to cross the placenta
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IgM
- make up ~ 10% of the serum anitbodies
- the first antibody produced during an immune response
- half-life of 5 days
- pentamer
- activate the classical complement pathways
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IgA
- make up~ 6% of the serum anitbodies
- half-life ~5 days
- found mainly in body secretion as secretory IgA where it protects interal body surfaces exposed to teh environment by blocking the attachment fo bacteria and viruses to mucous membrane
- provides passive immunity to baby in mother's milk
- made primarily in the mucosal- associated lymphoid tissue
- appears mostly as a dimer 2 "Y" shaped tissues
- secretory component to protect it from digestive enzymes in the secretion
- fc protion of secretory IgA binds to component of mucous
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IgE
- makes up ~0.002% of the serum antibodies w/ a half-life of 2 days
- tightly bond to basophils and mast cells via its Fc region
- monomer
- response to parasitic worms; ofter made in response to allergen
- protect external mucosal surgaces by promoting inflam, enabling IgG, complement proteins, and leucocytes to enter the tissues
- Fc portion of IgE can bind to mast cells and basophils where it mediates amny allergic reactions
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Major histocompatibilty Complex- I (MHC)
- found in all nucleated cells
- hold onto components that signal damaged or diseased
- cancer cells or virus infected cells can be noticed and destroyed w/ this method
- send a 'kill me' signal to other cells
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Major histocompatibilty complex- II (MHC)
- these are HLA's
- will hold onto the antigenic 'pieces' of engulfed organisms
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Ab production
- A. young B cell has prototype of Ab's on surface; find and internalizes the anitgen
- B. tell cell line must be found by an APC
- 1.Helper T cells (and maybe) APC find B cells and cause B cells to proliferate
- C.Cells use MCH II to recognize each other
- D. release of chemical signals from activated T cell cause repsonses in B cells
- E.B cell divides making plasma cells, and memory B cells for use later
- F. massive amounts of Ab's produced per second
- G. finding righ B cell/stimulation can take 5 days to 2 weeks
- H. next exposure will cause even greater amounts of Ab's to be made at a faster rate
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Cell mediated immunity (CMI)
- A.Involves T cells and not Ab production
- including helper T cells, cytotoxic T cells, memory T cells, and regulatory T cells
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Helper T cells
stimulate T and B cell mitosis and activation (thus leads to increase Ab production)
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cytotoxic T cells
- use enzymes like perforin
- also make an interleukin which acts as a migration inhibiting factor for macrophages
- TNF: tumor necrosis factor
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memory T cells
- watchdogs; wait until next exposure and initiate the T cells recall response
- send out chemotactic signal for variety of cells
- will proliferate into various kinds of T cells
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regulatory T cells
- slow down response
- causing a little bit of negitive feedback
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Type I hypersensitivity
- allergies
- Sx: localized vs. systemic
- response involved IgE, mast cells and eosinophils
- details of degranulation:
- mast cell or basophil releases histamine and other compounds that lead to sx such as: vasodilation, increase mucous membrane production, bronchial tube constriction inflammatory responses, eosinophils release anit- histamines
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What factors will determine the degree of a Type I reaction?
amount of IgE, # of mast cells vs. # of eosinophils, IgG levels, where Ag enters the body, how much Ag enters
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Treatment of Type I
anti- histamines, immunosuppressants, may need epinephrine in systemic reactions, try to raise IgG levels as blocker antibody, take anti- leukotryenes
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Type II
- cellular antigen source is destroyed; cytotoxic
- 1.complement fixation by IgG or IgM leads to cell lysis
- ex: transfusion reaction, transplant rejection, erythroblastosis fetalis
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Type III
- immune complex disorder
- 1.Make Ab's against own tissues; systems ability to recongize self is flawed
- 2. large #s of Ab's lead to inflammatory responses in tissue and compliment fixation
- 3. Ex: RA, lupus
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Type IV: Delayed hypersensitivity
- takes one to two days fro sx
- sx are more prolonged
- damage is due to too many macrophages being called to the are (self- destruction results)
- contract dermatitis: poison ivy
- IDD: destruction of beta cells by cytotoxic T cells
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