1) Chapter 19: Inflammation and the Immune Response

Antibody Classification IgA

-"secretory" antibody that forms a dimeric (two antibody group) structure -present in high concentrations in the secretions of mucous membranes and in the intestinal mucosa -very low circulating levels -most responsible for preventing infection in the upper and lower respiratory tracts, the GI tract, and genitourinary tract

Changes in Immune Function r/t Aging

-Component: Antibody-mediated immunity -Changes: total number of colony-forming B-lymphoctes and stability diminished, decline in natural antibodies, decreased response to antigens, reduction in amount of time antibody response is maintained -Nursing implications: less able to make new antibodies thus they receive immunization (flu shots), may not have sufficient antibodies present thus they need to avoid viral infections and receive "booster" shots

Changes in Immune Function r/t Aging

-Component: Cell-mediated immunity -Changes: thymic activity decreases and number of circulating T-lymphocytes decreases -Nursing implications: skin tests for TB may be falsely negative, more at risk for bacterial/fungal infections (respiratory tract, GI tract)

Changes in Immune Function r/t Aging

-Component: Inflammation -Changes: probable defect in neutrophil function, leukocytosis (increase in WBc) DOES NOT occur during acute infection, may not have fever during inflammatory/infectious episodes -Nursing implications: neutrophil counts may be normal, but activity reduction increases risk for infection, pt. have an infection but not show expected WBC, minor infections may be overlooked until severe infected/sepsis occurs

Activity of Interleukin 2 (IL-2)

-Increases growth and differentiation of T-lymphocytes -enhances natural killer cell activity against cancer cells

3 processes needed for protection from immunity**

-Inflammation -Antibody-mediated immunity -Cell-mediated immunity

Tissue Macrophages

-Lung: alveolar macrophage -Connective tissue: histocyte -Brain: microglial cell -Liver: Kupffer cell -Peritoneum: peritoneal macrophage -Bone: osteoclast -Joint: synovial Type A cell -Kidney: mesangial cell

Inflammation

-Protection is immediate but short-term against injury/invading organisms -Does not provide true immunity on repeated exposure to the same organisms -Is a NON-SPECIFIC body defense to invasion/injury and can be started quickly by almost any event, regardless of where it occurs or what causes it

WBC count normals

-Segs: 62%, 6,200/MM3 -Bands: 5%, 500/MM3 -Monos: 3%, 300/MM3 -Lymphs: 28%, 2,800/MM3 -Eosins: 1.5%, 150/MM3 -Basos: 0.5%, 50/MM3

3 Stages of Inflammatory Response**

-Stage I: Vascular part d/t histamine/serotonin/kinins to increase artiorle flow (blood vessels dilate > nutrients flow > capillary leak > warmth/redness/edema) MACROPHAGE deployment -Stage II: Neutrophilia phase (count can increase 5x normal in 12 hours) cellular exudate part (increased NEUTROPHILS > tissues secrete cytokines > exudate (pus) forms) -anti-inflammatory drugs work in this phase! -if this phase lasts more than a few days we she shift to bands! pg. 307 -Stage III: Tissue repair phase (new blood vessel growth/cell growth > scar forms) increased temp, WBC, ESR-erythrocyte sedimentation rate

5 Manifestations of Inflammation

-Warmth -Redness -Swelling -Pain -Decreased function

Hyperacute rejection

-begins immediately on transplantation -antibody mediated response -blood clots are formed throughout the new organ -most common in kidneys -Multiple pregnancies and blood transfusions greatly increase the risk of a hyperacute rejection!!!

When to say no to vancomycin

-broad spectrum antibiotic -last resort -started quickly to treat infection, but once we know what infection is- target control -prevent VRE (vanco resistance)

Antibody Classification IgG

-composes at least 75% of circulating antibody population -is heavily expressed on second and subsequent exposures to antigens -is greatly responsible for providing sustained, long-term immunity against invading microorganisms -activates classic complement pathway, enhancing effectiveness of neutrophil and macrophage phagocytosis -involved in the antibody-dependent cell-mediated non-self cell killing action of natural killer cells

Antibody Classification IgM

-first antibody formed by a newly sensitized B-lymphocyte plasma cell -composes about 10% - 15% of circulating antibody population -especially effective at the antibody actions of agglutination and precipitation -largest antibody molecule forming a pentomeric (five antibody group) structure w/ 10 potential binding sites -activates classic complement pathway

Human Leukocyte Antigens (HLAs)****

-found on the surface of all body/liver cells that a person and serve as a "cellular fingerprint" for that person -determine tissue type of person -unique proteins **identical only with identical siblings -because the cell surface proteins are "non-self" to another person's immune system, they are antigens capable of **stimulating the immune response (could be bacteria, or wrong unit of blood) -have about 40 major HLAs; make up major histocompatibility complex (MHC) -inherit from parents -WHEN ENCOUNTER ANOTHER HLA IF NOT A PERFECT MATCH, INFLAMMATION IS INITIATION

Tumor Necrosis Factor (TNF)

-induces fever -major cytokine involved in rheumatoid arthritis damage -major cytokine involved in the acute inflammatory response to infectious bacteria and starts many of the systemic complications of severe infection or sepsis -increases leukocyte adhesion -participates in graft rejection -induces cachexia and muscle breakdwon -induces cell death -stimulates delayed hypersensitivity reactions and allergy

Activity of Interleukin 1 (IL-1)

-induces fever -stimulates production of prostaglandins -increases growth of CD4+ T cells

Sandimmune therapy

-medication for the rest of pt.s life -must undergo regular kidney function tests -gums may become swollen

Purpose of inflammation/immunity

-neutralize organisms -eliminate organisms -destroy organisms

Acute rejection

-occurs w/in 1 - 3 months after transplantation -Antibody mediates results in vasculitis in new organ -Cellular releases cytotoxic T cells and NK cells to the organ -does not always mean that person will lose the organ (treatments can reduce immune reponses)

Antibody Classification IgD

-present in low blood concetration -co-expressed w/ IgG -acts as a receptor on unsensitized B-lymphocytes

Leukocyte functions ***

-recognition of self versus non-self!! -destruction of foreign invaders, cellular debris, and unhealthy/abnormal self cells -production of antibodies directed against invaders -complement activation -production of cytokines that stimulate increased specific leukocyte activity

B cells

-responsible for Antibody-mediated immunity -can only respond to one specific type of antigen -Activated B cells divide into plasma and memory cells -Plasma cells secrete antibodies -Memory cells are dormant

Chronic rejection

-similar to chronic inflammation/scarring -smooth muscles of blood vessels overgrow/occlude organ vessels -good control, but NO CURE

Body defenses to prevent entrance of organisms

-skin -mucous membranes -normal flora -natural chemicals that inhibit bacterial growth

Activity of Interleukin 6 (IL-6)

-stimulates liver to produce fibrinogen and protein C -increases rate of bone marrow production and stem cells -increases numbers of sensitized B-lymphoctes

Antibody Mediated Immunity (humoral)

-to get the pathogens that have yet to infect cells (extracellular) -Employs Helper T cells & B cells -B cells will produce antibodies -B cells need signals from Helpter T cells that needs to hear from a macrophage that there's been an invasion (cellular-mediated) -Interleukin 2 acts as a signal to B cell that has already been primed to pathogen -B cell initiates cell division that arises to army of B-cell that fights off infection -Half of B cells become effector cells and others become memory -Effector cells produce massive quantities of specifically shaped antibodies that then bind to pathogen -Antibodies bound to pathogen mark them for destruction by macrophages

Rescue therapy

-used to treat acute rejection episodes -can be used w/ or in place of maintenance drugs -Antilymphocyte globulin (ALG) given short period of time to clear lymphoctes from body

Antibody Classification IgE

-variable concentration in blood -associated w/ antibody-mediated hypersensitivity reactions -binds to mast cells and causes their degranulation when an allergen (antigen) binds to IgE antigen recognition sites

Immunocompetent

-when all the different parts/functions of inflammation and immunity are working -person has maximum protection against infection

Inflammation Step

1. Injury 2. Inflammation mediators released: histamine, kinins, etc. 3. Vasodilation (heat) 4. Increase permeability of blood vessel walls so chemotaxis can occur 5. Clot forms 6. Phagocytosis

Cell Mediated Immunity Process

1. Macrophage engulfs pathogen & becomes antigen-MHC complex 2. Helper T cell binds to antigen-MHC complex 3. Cytotxic T cells binds as well & becomes primed recognizing specific antigen 4. Macrophage releases IL-1 stimulating Helper T cell 5. Helper T cell releases IL-2 & causes Cytotoxic T cells to divide into army of cells 6. Four specific T cells created: -Killer T cell: seek to directly destroy antigen -Helper T cell: stimulate the T & B cells & enhance immune system -Supressor T cell: inhibit immune response when antigen has been destroyed -Memory T cell: remember antigen

Infection Disease Process Cycle (exam)

1. susceptible host 2. portal of entry 3. mode of transmission 4. portal of exit 5. reservoir 6. causative agent

Immune function declines starting in our

30s

Neutrophils

< 500 r/t radiation, chemotheraphy > 70% of total WBC r/t bacterial infection neutrophils comprised of more bands: shift to left: infectious process going on for longer period of time

Lymphocyte

<1,000 expect pt. to be on steroids, immunosupressant drugs, HIV tx, renal disease >5,000 r/t virus or immune disease

Total WBC

<5,000 r/t disease or treatment affecting marrow >11,000 r/t inflammation, infection, sepsis, trauma >100,000 r/t leukemia

Bands

> 5% of total WBC: large scale infection or inflammation

Monocyte

> 500 r/t fungal infection, mono (epstein-barr virus), chronic inflammatory disease

Liver Lab Tests

Abnormalities occur only after significant damage AST, ALT, Alkaline phosphatase, GGT, PT/PTT, Mag, Bili, Albumin, ammonia

7 Steps of AMI (antibody mediated immunity) are needed to produce a specific antibody directed against a specific antigen whenever the person is exposed to that antigen: [BOOK VERSION]

B-CELLS!!! -Exposure/invasion: new antigens stimulate immune response -Antigen recognition: B-cell recognizes non-self -Sensitization: B-lymphocyte becomes aware of antigen & presents to helper T cell. Each B-cell can be sensitized to only one type of antigen. - After the B-cell is sensitized, it divides and produces a plasma cell which starts to immediately proce antibodies. The other is a memory cell or sensitized B-cell but does not start to function until the next exposure to the same antigens -Antibody production: antibodies produced by plasma cells search out specific antigens-specific to the antigen sensitized by parent B cell -Antibody-antigen binding: immune complex formed -Antibody binding actions: triggered by binding of antibodies to antigens -Sustained immunity: memory of antigens in specific antibodies

B-lymphocte function

Becomes sensitized to foreign cells and proteins (ANTIBODY-MEDIATED)

Cytokines

Cell-mediated immunity (CMI) regulates the immune system by the production and activity of cytokines -produced by WBCs -cytokines act like "messengers" that tell specific cells how and when to respond -cytokines include the interleukins, interferons, colony-stimulating factors, and tumor necrosis factor

Monocyte function

Destruction of bacteria and cellular debris; matures into macrophage (INFLAMMATION) -circulating phagocytes -2-8% of WBC

Helper/inducer T-cells

Easily recognize self cells versus non-self cells. In response to the recognition of non-self (antigen), helper/inducer T-cells secrete LYMPHOKINES that can enhance the activity of other WBCs.

Helper/Inducer T-Cell function

Enhances immune activity through secretion of various factors, cytokines, and lymphokines (CELL-MEDIATED)

Shift to the left

Mature neutrophils could be all consumed in an infection, when they are all gone.. the individuals neutrophils goes down but the bands increase to compensate. they cannot take part in phagocytosis until they mature

Transplant Rejection

Natural killer (NK) cells and cytotoxic/cytolytic T-cells also destroy cells from other people or animals.

Natural killer cell function

Non-selectively attacks non-self cells, especially body cells that have undergone mutation and become malignant, also attacks grafts and transplanted organs (CELL-MEDIATED)

Neutrophil functions

Non-specific ingestion and phagocytosis of microorganisms and foreign protein (INFLAMMATION) mature neutrophils: segmented or polymorphonuclear cells -it takes 12-14 days for a stem cell to grow into a mature neutrophil -lifespan: SHORT 12-18 hours -55-70% of total WBC -100 billion released from bone marrow daily **EACH NEUTROPHIL CAN TAKE PART IN ONLY ONE EPISODE OF PHAGOCYTOSIS & THEN IT IS EXHAUSTED**

Macrophage function

Non-specific recognition of foreign proteins and microorganisms ingestion and phagocytosis (INFLAMMATION)

Basophil function

Releases histamine and heparin in areas of tissue damage (INFLAMMATION) -0.5% of total WBC, release vasoactive mediators that cause manifestations of infection

Memory cell function

Remains sensitized to a specific antigen and can secrete increased amounts of immunoglobulins specific to the antigen on re-exposure (ANTIBODY-MEDIATED)

Lymphocyte functions

Respond to viral infections (VIRAL) -28% of WBC

Plasma cell function

Secretes immunoglobulins in response to the presence of a specific antigen (ANTIBODY-MEDIATED)

Cytotoxic/cytolytic T-cell function

Selectively attacks and destroys non-self cells, including virally infected cells, grafts, and transplanted organs (CELL-MEDIATED)

Cell-mediated immunity (CMI)

T-CELLS!!! -To get rid of already infected body cells (intracellular) -employs Helper T cells & Cytotoxic T cells -Helper T cells release lymphokines (IL) -lymphokines increase bone marrow production of stem cells and speed up their maturation -non-self cells most recognized by CMI: cancer cells, infected self cells

Adaptive Immunity

The ability to recognize and remember specific antigens and mount an attack on them. Humoral (B cells) and cell-mediated immunity (T cells) are examples. [antibody-mediated immunity]

Organization on the Immune System

The bone marrow is the source of all blood cells, including immune system cells. -The bone marrow produces immature, undifferentiated cells called stem cells -PLURIPOTENT: more than one potential outcome -Outcome is base upon the bodies needs ex. stem cell exposed to erythropoitin will become a RBC

Active Immunity

The type of immunity when an individual makes his or her own antibodies after being ill and recovering or after being given an immunization or vaccine

Liver Functions

Vascular Functions -Blood Storage -Blood Filtration - Kupfer cells Secretory Functions -Bile salt production -Conjugation and secretion of bilirubin -Cholesterol removal

Eosinophil function

Weak phagocytic action; releases vasoactive amines during allergic reactions (INFLAMMATION) -kill by process of degranulation -kill microbes that are too large for phagocytosis (parasites) -1.5% of total WBC

Optimal function of CMI requires

a balance between helper T-cells and suppressor T-cells. This balance occurs when helper T-cells outnumber suppressor T-cells by a ratio of 2:1.

Inflammation does not always mean that

an infection is present.

KPC bacteria

completely drug resistant

Maintenance therapy

continuous immunosuppression used after a solid organ transplant -drugs -monoclonal antibodies -cancer therapy drugs

The immune cells are the only cells capable of

determining self from non-self

Stem cells are PLURIPOTENT

each cell has more than one potential outcome- when the stem cell is first created it is undifferentiated. the type of mature cell that stem cells becomes depends on which pathway it follows.

NOT NOSOCOMIAL INFECTIONS

hospital acquired infections Most common sites: Urinary tract (catheters) Surgical wounds (mediastinal!!!!) Ventilation associate pneumonia Central Line

Bands (Stabs)!!

immature neutrophils ineffective at phagocytosis

Erythropoietin

increases growth and differentiation of erythrocytes

Thrombopoietin

increases growth and differentiation of platelets

Granuloctye Macrophage-Colony Stimulating Factor (GM-CSF)

increases growth and maturation of myeloid stem cells

Granulocyte Colony-Stimulating Factor (G-CSF)

increases number and maturity of neutrophils

Absolute neutrophil count (ANC)

measurement revealing proportion of neutrophils that can be utilized in first response immune interactions. >1500 = normal immune defense the higher the numbers, the greater the resistance to infection

MRSA is most prevalent in

patients in long-term care facilities -in nostrils commonly -lesions like spider bite (first question ask if they remember being bitten by spider).

Supressor T cells

prevent hypersensitivity (immune overreactions) on exposure to non-self cells or proteins. This function is important in preventing the formation of antibodies directed against normal, healthy self cells, which is the basis for many autoimmune diseases Balance elicits protection when helper or inducer T-cells outnumber suppressor T-cells by a ratio of 2:1.

Antigens

proteins capable of stimulating the immune response

Self-tolerance

recognizing self from non-self body cells (cancer cells, cells from other people, infected body cells, & invading organisms) which is necessary to prevent healthy body cells from being destroyed The client who is exposed to invaders recovers rapidly after the invasion without damage to healthy body cells.!!!!!!

Passive Immunity

when antibodies against an antigen are in a person's body but were not created there. Rather, these antibodies are transferred to the person's body after being made in the body of another person or animal. (breastmilk)