Phys And Pathophys - Infection, Immunity, Allergic Response And Coagulation

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immunity definition

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is the body's ability to resist almost all types of organisms or toxins that damage organs and tissues

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components of the immune system

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thymus, lymph nodes, tonsils, spleen, and WBC production by the bone marrow

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our bodies combat different infectious agents and toxins by

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WBC and tissue leukocytes directly destroying invaders via phagocytosis, and by stimulating the production of antibodies and sensitizing lymphocytes to destroy invaders with repetitive exposure

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types of immunity

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active and passive

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types of active immunity

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naturally acquired and artificially acquired

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types of passive immunity

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naturally acquired and artificially acquired

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innate immunity is

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general processes that were put into place before exposure - ie - phagocytosis, stomach acid, skin, lysozymes, complement cascade, matural killer cells (anything naturally acquired)

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adaptive immunity is

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includes the production of antibodies upon exposure to a toxin or activation of lymphocytes

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fetal immunity occurs by

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maternal antibodies travel across the placenta to the fetal circulation. antibodies are also found in breast milk.

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fetal passive immunity lasts for

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several weeks

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example of passive immunity

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maternal-fetal antibodies

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organs of the immune system

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tonsils and adenoids, lymph nodes, lymph vessels, spleen, thymus, peyer's patches, appendix, bone marrow

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describe lymphocyte growth

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originate in embryonic lymphocyte committed stem cells in bone marrow (in utero), then travel to the thymus gland where they are processed for diversity and specificity until there are thousands of different T lymphocytes. they then leave and are spread via the blood to all the tissues

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describe thymus function

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process and develop diversity and specificity of lymphocytes for specific antigens. It also makes sure the antigens are not self reactive by releasing a small amount of each batch to see if self reactive, and destroys 90% of them because they are self reactive

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removal of the thymus gland shortly after birth allows for

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better organ transplant rates

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B lymphocytes are made by

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the liver and the bone marrow

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B lymphocyte function

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actively secrete antibodies which are large protein molecules that bind to and destroy the antigens.

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are B or T lymphocytes more diverse?

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B lymphocytes

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B lymphocytes are commonly found

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in the lymph nodes

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when an antigen binds to a specific T and B lymphocyte then

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the T lymphocyte is more active, forms substances and T helper cells which help activate the B cells

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describe cell line genesis of WBC's

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the pleuripotential hematopoietic stem cell differentiates into the myelocyte and lymphocyte

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platelet genesis

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granular fragment of another cell line

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WBC's and platelets are stored

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in the bone marrow

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lymphocytes are stored

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in the lymph tissue

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6 types of WBC

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neutrophils, eosinophils, basophils, monocytes, lymphocytes, and plasma cells

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normal % for neutrophils

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62%

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normal % for eosinophils

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2.3%

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normal % for basophils

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0.4%

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normal % for monocytes

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5.4%

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normal % for lymphocytes

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30%

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life span of a WBC is

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4-8 hours in the blood and 4-5 days in the tissue - dependent on how active it is and lifespan is greatly reduced when at war

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what blood cells destroy stuff in the tissue

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neutrophil and macrophages

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neutrophils work by

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being aggressive mature warriors that attack and destroy invaders, even in the blood

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macrophages life story

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baby macrophages are monocytes that float through the blood stream, when they enter the tissue they swell and become macrophages. they can live for months in tisue

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lymphocyte life span

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weeks to months

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lymphocytes enter circulation via

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the lymph

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how do WBC's enter the tissue

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diapedesis, being drawn toward invaders via chemotaxis

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eosinophil's specialty

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parasitic infections

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eosinophil's are described as

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weak phagocytes and a small % of WBC

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Basophils are similar to

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mast cells

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basophils contain

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heparin, histamine, bradykinin, and seratonin - plays a role in allergic reactions

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platelets circulate for

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12 - 14 days

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what cells are professional eaters

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neutrophils and macrophages

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why don't phagocytes eat everything they encounter?

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natural structures are smooth so are hard for the phagocyte to grab on, natural body structures have a protective protein coat that repels phagocytes (dead and foreign tissue do not), immune system antibodies adhere to invaders producing the compliment cascade and "calling in the dogs" (labels the particle for destruction)

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macrophages are located everywhere but tend to hang out in what tissues

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those most exposed to invaders - brain, lungs, liver, kidney, lymph nodes, spleed, blood, bone marrow, joints

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the monocyte-macrophage cell system is aka

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the reticuloendothelial system

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the monocyte-macrophage system is present

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in all tissues

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the monocyte-macrophage system also helps by

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removing some drugs from the body

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the monocyte-macrophage system in the skin and SQ tissue is

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the histocytes

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the monocyte-macrophage system in the lymph nodes

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tissue macrophages

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the monocyte-macrophage system in the lungs are

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alveolar macrophages

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alveolar macrophages work by

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becoming giant cells and forming capsules around substances that take a long time to digest - if ever (TB)

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the monocyte-macrophage system in the liver

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kupffer cell

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the monocyte-macrophage system in the spleen and bone marrow

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splenic pulp

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characteristics of inflammation are

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vasodilation of the local blood vessels (erythemia), leaky capillary beds (edema), interstitial space clotting (fibrin), granulocytes and monocytes move in, tissue releases chemicals (histamine, bradykinin, serotonin, prostaglandings, complement system, blood clotting proteins (all causing additional swelling, edema, capillary leak and pain!)

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goal of inflammation is to

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wall off the area

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intensity of the inflammation is dependent on

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the degree to which the invader causes normal tissue damage

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staphylococci bacteria kill tissue by

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producing letal cellular toxins - leading to rapid inflammation and defense against staph

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does strep or staph produce a more intense inflammatory response

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staph

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is strep or staph more dangerous

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strep - because slower immune response allows bacteria to spread farther before body combats it

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what happens to the macrophages and neutrophils -

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they eat themselves to death - they ingest lots of bacteria and then die

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pus is formed by

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necrotic normal tissue and dead macrophages

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abscesses and pimples are most likely caused by

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staph

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substance P causes

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pain - revs up pain sensation receptors

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components of an antibody

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light chain, heavy chain, antigen-binding region, constant region

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antibodies aka

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gamma globulins called immunoglobulins (Ig)

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Ig make up what % of plasma proteins

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20%

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Immunoglubulins are made of

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light and heavy chain polypeptides

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5 classes of antibodies are

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IgM, IgG, IgA, IgD, IgE

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methods of antibody attack are

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lysis, neutralization, precipitation, agglutination

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problem with antibody defense

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quite slow

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agglutination is

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when many antibodies cluster around an antigen rendering it ineffective

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precipitation occurs when

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so many antibodies cluster together with the antigen that it is no longer soluble

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neutralization is when

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antibodies cover the toxic sites on an antigen making the antigen ineffective

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lysis is when

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antibodies rupture the cell wall of the antigen

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describe the compliment cascade

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a group of about 20 proteins, many of which are enzyme precursors, that are triggered to act when an antigen binds to an antibody exposing the C-1 molecules binding site

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events of the compliment cascade include

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increasing the phagocytic activity of neutrophils, macrophages, increasing the # of bacteria these guys can eat - lysis of bacterial walls - changing invaders surface to allow adhesion - attack viruses - initiate chemotaxis - activate mast and basophils to increase local blood flow - and contribute to local inflammation

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cancer an complement cascade

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many cancer tx can be based on specific points of the complement cascade

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types of T cells

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memory, cytotoxic (aka killer cells), supressor, helper

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memory cells job

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remember an antigen exposure so that the next time you see that antigen the response time is much faster (blueprint)

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cytotoxic t cells

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go to war and destroy the invaders

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suppressor T cells

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suppress T cell activity

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helper T cells regulate

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many different immune system functions through the use of lymphokine mediators

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examples of lymphokine mediators regulated by T helper cells

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interleukins 2,3,4,5,6,7,9, and Interferon, and granulocyte-monocyte colony stimulating factor

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without T cells - the immune system

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shuts down entirely

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AIDS kills patients by

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destroying or inactivating the T helper cells

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natural killer cells role is to

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attack the body's own cells that have been infected and potential cancer cells - also plays a role in apoptosis

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natural killer cells work by

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creating an antibody bridge to the cell, then secreting perforin that makes holes in the membrane of the cell, with enough holes the water rushes in and the cell will swell and die (sometimes too much calcium entering cell will trigger apoptosis)

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IgE antibodies attach to

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mast cells and basophils

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how do allergies work

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a primary exposure causes a cascade and development of IgE antibodies. the IgE antibodies attach to mast cells and basophils. Then with repeat exposure the antigen binds to the IgE antibody causing a breakdown (degranulate) in mast and basophil membranes and release of mediators producing symptoms (histamine, seratonin, bradykinin, etc)

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difference between anaphylactic and anaphylactoid reactions

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anaphylactic reactions require antigen-antibody complexing - anaphylactoid does not (no previous exposure needed)

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anaphylaxis is

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a life threatening manifestation of antigen-antibody interactions - an exposure to an antigen results in explosive degranulation of mast cells and basophils. Initial symptoms within 10 minutes (rash and itching)

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what 2 events associated with anaphylaxis leads to cardiac collapse and death

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profound vasodilation and profound loss of intravascular fluid

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anaphylaxis contributors to respiratory compromise

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laryngeal and bronchial edema

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anaphylaxis treatment goals

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reversal of arterial hypoxemia, replacement of intravascular volume (1-4 liters), vasopressors for CV support, and inhibition of reaction (epi)

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epi doses for anaphylaxis

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10 - 100 mcg IV then double and repeat every 1 - 3 minutes until SBP is adequate (SQ 0.3 - 0.5 mg 1:1000)

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epi works to combat anaphylaxis by

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increasing intracellular CAMP which restores membranes, relaxes bronchial airways

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non life threatening anaphylaxis treatment is

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oxygen, antihistamines, corticosteroids, beta 2 agonists

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benadryl dosing for mild anaphylaxis

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50 - 100 mg IV

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in addition to benadryl, also give what for anaphylaxis

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a histamine 2 blocker like zantac or pepcid

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in or - first signs of anaphylaxis were

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no pulse, bronchospasm, flushing, rash, hypotension

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under anesthesia, anaphylaxis is

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either hard to recognize, or people go down much harder and faster

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treatment for anaphylactoid reactions

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same as for anaphylaxis - same symptoms - can be just as bad as anaphylaxis - no need to differentiate for treatment

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most fatal anaphylactic drug reactions are from

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penicillin

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drug sensitivity accounts for what % of OR deaths

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4.3% of anesthesia related deaths in the UK

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presentation of latex allergy

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within 30 minutes

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presentation of drug allergies

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within 10 minutes

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of anesthetics - which drugs that we use are most likely to cause allergic reactions

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muscle relaxants - watch for cross sensitivity with other relaxants

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a large histamine release is caused by

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some muscle relaxants (succs)

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angioedema is

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a rare autosomal dominant disorder due to decreased functional activity of the plasma compliment C-1 esterase inhibitor.

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angioedema presents as

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inadvertant swelling - sometimes life threatening

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trigger for angioedema

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emotional stress in 40 - 50% of cases

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angioedema attacks last

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48 - 96 hours

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most dangerous part of angioedema is

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laryngeal edema

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treatment for angioedema is

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long term steroids

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angioedema is seen by anesthesia for

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an emergency airway with back up tracheostomy plans - and for planned surgeries - watch for high dose steroids and concentrated C-1 (which is found in FFP)