Pathophysiology Exam One--Inflammation And Immunity

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inflammation

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nonspecific beneficoal defense mechanism when body tissue is injured

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causes of inflammation

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anything that damages tissue

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what does the inflammatory response do?

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neutralizes the causative agent, cleans up the damaged tissue and makes it suitable for repair

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cardinal signs of inflammation

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rubor, calor, dolor, tumor, altered function

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rubor

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redness, creased blood flow--hyperemia, controlled in part by histamine

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calor

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heat. On the surface of the body the inflammed area feels warmer

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dolor

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pain, caused by chemical changes in the inflammed site and by swelling

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tumor

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swelling, local swelling at site caused by fluid and cells moving from capillaries to interstitial tissue (exudate)

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movement of fluid in inflammatory response

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increase in the permeability of capillary and small vessel walls leads to protein protein and fluid leakage, also increased flow of lymph through the lymphatic system

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movement of cells in inflammatory response

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blood becomes more viscous as fluid is leaked out into the injured area, cellular portion of the blood (RBC and WBC) adhere to the lining of the vessels (margination) and the WBCs begin to move out to the injured tissue

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chemotaxis

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chemical signal in the injured tissue that attracts WBCs

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mediation of the inflammatory response

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histamine released and plasma factors are activated

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what happens when histamine is released?

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histamine stored in mast cells, when mast cells injured histamine is released and vasodilation and increased vascular permeability occur

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where is histamine stored

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mast cells

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what happens when plasma factors are activated?

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they become vasoactive, some release histamine and some are chemotactic agents

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Patterns of inflammation

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acute, chronic and subacute

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acute inflammation

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sudden onset, if it clears up normally there is no residual damage

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chronic inflammation

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goes on for months or years, causes a lot of damage, release of WBC and enzymes (which can damage cells as well)

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subacute inflammation

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may not show S/Sx but the chronic response to it causes enzyme damage

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neutrophils in inflammatory response

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polymorphonuclear neutrophils (PMNs) appear early in the exudate, first responders-start cleaning up debris, die and join the exudate, they engulf (phagocytosis) kill and digest the causative agent through the release of enzymes

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WBC in inflammatory response

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neutrophils, eosinophils, basophils

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eosinophils in inflammatory response

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respond esp to allergic reactions and parasitic infections

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basophils in inflammatory response

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contain histamine and heparin--important immune responders

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Monocytes in inflammatory response

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2nd responders--slow moving with longer life than neutrophils (PMNs), move into area of inflammation in the exudate where they are called macrophages--phagocytic and can kill and digest various agents, found in sites other than in area of inflammation--fixed macrophages in liver, spleen and lymph system

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suystemic aspecs of inflammatioon

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fever, leukocytosis (increased release of WBCs), malaise, anorexia, elevated pulse and resp rate

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immunological response

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certain foreign materials when introduced into the body cause a change in the host so that subsequent responses to the foreign material (antigen) cause a diff reaction than the first exposure, protective response to rid the body quickly of foreign material, lymphocytes are sensitized to antigens

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Antigens

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usually Ig proteins

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rules of an intact immune system

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immune response mounted against only foreign (antigenic) material, response is more rapid with repeated exposure (memory), response of antibodies is specific to the specific antigen

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lymphocytes

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greatly vary in size and function, concentrated in lymphoid tissue, move through blood and lymph

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where are lymphocytes manufactured?

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in bone marrow

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T lymphocytes

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migrate through the thymus, as they move through the body they diferentiate into helper cells, suppressor cells, and killer cells

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B lymphocytes

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not under the influence of the thymus, can change into plasma cells which produce immuoglobin antibodies

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Null cells

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have receptors for IgG

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NK cells

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natural killer cells can destroy tumor cells

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antibody mediated response

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b lymphocyte response, creates the antibodes for the next exposure so that the reaction time is quicker on second exposure

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Active immunization

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infected by or injected with and antigen and form either antibodies or T lymphocytes, on subsequent exposure you have a more rapid response--memory cells

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Passive immunization

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antibodies manufactured elsewhere and transferred to the body, short lived, no memory EX: breast milk, injection of gammaglobulin to temporarily boost immunity

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Types of immunoglobulins or antibodies

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IgG, IgA, IgM, IgE

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IgG

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circulating and important in resistanceto infection and passive resistance for a fetus, surveilance antibody

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IgM

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early reactors to antigens

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IgA

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found in mucosal surfaces

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IgE

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attached to mast cells and help with release of histamine-allergic reactions

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complement system

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inactive proteins that are activated by antigen-antibody interaction, these activated proteins strengthen the speed and strength of the immune response so that the antigen is neutralized more quickly

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How does the complement system amplify the immune response?

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alters the cell membrane of the antigen to lead to lysis, causes release of histaminefrom mast cells increasing vascular permeability. Increases migration of leukocytes-chemotaxis

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cell mediated immunity

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does not produce antibodies but is mediated by T lymphocytes that have become specifically reactive to a particular antigen when exposed for the first time, release lymphokines which increase the # and efficiency of macrophages for destruction of the antigen, not passively transferred by vaccination

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anaphylactic reaction

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type I reaction, on first exposure to the antigen the IgE antibodies are made and attach to mast cells, second exposure rapid release of histamine in mast cells

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what does histamine do in an allergic reaction?

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vasodilation and increased capillary permeability--swelling and redness, if large amount of antigen introduced or subject is very sensitive then release of histamine is massive and wide spread --bronchiolar constriction and suffocation

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Type IV hypersensitivity reaction

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cell mediated involving sensitized T lymphocytes EX: contact dermatitis and rejection of foreign grafts (transplants)

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autoimmunity

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the body loses tolerance to own tissue and begins to recognize own cells as the antigen--'self' immunity, losses track of what is foreign and what is self

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normal responses to infectious agents

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transmissibility--direct (coughing, sneezing, touching), indirect (though soil, inanimate objects, food, water, insects, exudates and excreta (blood and body fluids)

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infection

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invasion of tissues by microorganisms

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virulence

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ease by which agent gets by defense mechanisms and rapidly causes disease

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defense mechanisms of the body against infectious agents

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intact skin and mucous membranes, GI tract, respiratory tract, inflammatory response

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bacteremia

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infection spread through the blood and lymphatic system--systemic

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septicemia

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large # of microorganisms in the blood --viral or bacterial

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opportunistic infection

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organisms that do not normally produce dz can do so if the hosts has compromised defense mechanisms, may happen through dz, medications,