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Chronic Exam 4

Exam 4

TermDefinition
Natural Immunity nonspecific immunity, present at birth. Similar response from one encounter to the next, distinguished "self" from "non-self." 3 types
Acquired Immunity not present at birth, develops after exposure to antigen (vaccines or contracting disease). 2 Types: Passive and Active
Bone Marrow produces WBCs; Lymphocytes that turn into B-cells or T-cells
B-cells produced and mature in bone marrow, then enter into circulation
T-cells made in bone marrow, mature in thymus and further divide into different types of cells
Spleen red pulp (where RBCs are destroyed) and white pulp. Acts as a filter, concentrations of lymphocytes here
Thymus distributes lymphocytes throughout body (head, neck, axillary, inguinal, tonsils, and adenoids)
Immune System network of cells, tissues, and organs that all help defend against foreign invaders. Remembers invaders from previous exposures.
Function of Immune System remove foreign antigens (viruses, bacteria, etc.) to maintain homeostasis.
Immunocompentant properly functioning immune system
Immunocompromised immune system that isn't functioning properly
How Natural Immunity Works coordinates initial response, produces cytokines, etc. that control pathogen by elimination OR promotes an acquired immune response. Happens in two stages: immediate or delayed
Immediate Natural Immunity within 3 hours of exposure
Delayed Natural Immunity 4-96 hours after exposure
Inflammatory Response responds to tissue injury or invading organisms. With chemical mediator assistance, minimize blood loss and and regenerates injured tissue
Physical Barriers intact skin, mucous membranes, cilia of respiratory tract
Chemical Barriers mucous, gastric secretions, enzymes in sweat and tears
Active Acquired Immunuity defenses developed by person's own body, lasts many years-lifetime, Ex. immunization or contraction of disease
Passive Acquired Immunity temporary immunity transmitted from source outside the body, used in emergencies for fast immunity Ex. hepatitis exposure, breast milk, needle-sticks
Body Response to Invasion 3 means of defense: phagocytic, humoral/antibody, cellular
Phagocytic Response 1st line of defense, involves granulocytes and macrophages (WBCs), has ability to ingest foreign bodies and destroy them, removes dead and dying cells, apoptosis occurs
Humoral/Antibody Response 2nd line of defense, begins with B-cells turning into plasma cells that manufacture antibodies. Antibodies (immunoglobulins;different types) match up with antigens (like lock and key).
IgG appears in serum, role in fighting off blood borne and tissue infection antigens. Enhances phagocytosis, makes up 75%
IgA appears in blood, saliva, tears, breast milk, tears, pulmonary, GI, and vaginal tissues. Protects against resp., gastro., gentro. antigens and infections. Prevents antigens from being absorbed from food. Passes through breast milk for protection
IgM appears mostly in intravascular serum, FIRST to be produced in response to bacterial and viral infections. Very effective in killing bacteria, 10% of total
IgD appears in small amounts in serum, possibly influences b-cell differentiation, remains attached to b-cell, plays key role in initiating early b-cell immune response
IgE appears in serum, takes part in allergic and hypersensitivity reactions, combats parasitic infection, small amount
Cellular Response 3rd line of defense. Stem cells leave bone marrow->thymus, become T-cells->t-cells patrol blood for antigens->antigen attaches to antigen receptor on T-cell->antigenic message sent back to lymph nodes->t-cell production stimulated
Helper T-Cell attacks foreign invaders, initiates inflammatory response. 2 types: helper T1 and helper T2
Helper T1 Cell increases activated cytotoxic t-cells
Helper T2 Cell increases b-cells antibody production
Suppressor T Cell suppresses immune response after battle with antigen
Memory T Cell remembers contact with antigen, when exposed again, mounts immune response
Cytotoxic (killer) Cell lyses cells infected with virus
Stages of Immune Response recognition, proliferative, response, effector
Recognition Stage antigens recognized by circulation lymphocytes and macrophages, lymphocytes send message to lymph node when antigen is detected
Proliferation Stage dormant lymphocytes proliferate and differentiate into cytotoxic (killer) t-cells or b-cells
Response Stage cytotoxic T & B cells perform cellular and humoral functions
Effector Stage Antigens destroyed through action of antibodies and cytotoxic T-cells
Primary Immunodeficiency genetic in origin, caused by defects in cells of immune system, represent inborn errors of immune function. Primarily seen in infants and small children, can be FATAL of not treated
Job's Syndrome (hyperimmunoglobulinemia) (Phagocyte immunodeficiency) white cells cannot initiate an inflammatory response to infectious organisms
S&S of Job's Syndrome increased bacterial infections, increased fungal infections, increased viral infections, deep seeded cold abscess (usually on lung/skin), eczema and dermatitis
Dx & Tx of Job's Syndrome nitroblue tetrazolium reductase test. Tx: infusion of granulocytes/macrophage CSF, infusions of blood/blood products, hematopoietic stem cell transplant
Nitroblue Tetrazolium Reductase Test (NTR) released nitroblue into WBCs, should turn them blue. If they turn blue, indicates that WBCs are killing bacteria
Bruton's Disease (B-cell immunodeficiency) sex-linked agammaglobulinemia. B-cells don't mature, all antibodies disappear from patient's plasma. Males at high risk. S&S: severe infections after birth, frequent respiratory infections. TX: immunoglobulin infusions
Common Variable Immune Deficiency (CVID) (B-cell immunodeficiency) hypogammaglobulinemia, more dysfunction that deficiency, produce decreased amounts of B-cells. Tx: IV immunoglobulin infusions
Digeorge Syndrome (thymic hypoplasia) (T-cell immunodeficiency) thymus gland fails to develop normally, leading to deficiency in production of t-cells. Genetic disorder, usually effects infants and small children. Dx; test T-cells. Tx; antibiotics
S&S of Digeorge Syndrome recurrent infections, HYPOCALCEMIA, facial & congenital heart disease. TX: oral ca+, vit.D, parathyroid hormone, transplantation of fetal thymus, bone marrow/stem cell transplant, immunoglobulin infusions
Secondary Immunodeficiencies more common than primary, frequently occur as result of underlying disease process of treatment of disease. Commonly caused by malnutrition, chronic stress, diabetes, exposure to immunotoxic meds (Benzene), chemicals, HIV & AIDS
Care of Client with Immunodeficiency h&p, ask about allergies, genetic disorders, chronic illnesses, immunizations, recurrent infections Teach: nutrition, O2, cough & deep breathing, incentive spirometer, preventing infection, oral care. Higher incidence in males
Types of Organ Rejection hyperacute, acute, chronic/long-standing
Hyperacute Rejection beings immediately, blood clotting cascade causes clots to form throughout organs, most common in kidney, organ is removed ASA dx'd
Acute Rejection Occurs within 1 week-3 months. Vasculitis and necrosis occurs
Chronic Rejection Organ becomes fibrotic over period of time, then organ can no longer function. Prevention and Tx: Immunosuppressants and cyclosporin
Granulocytes Neutrophils, basophils, eosinophils. Help fight invasion by engulfing foreign bodies, releasing cell mediators (histamine, bradykinin, prostaglandins)
Neutrophils first leukocytes to arrive at site of inflammation
Basophils and Eosinophils increase in allergic or stress reactions
Agranulocytes Monocytes (phagocytic) engulf, ingest, destroy more foreign bodies than granulocytes. Macrophages (phagocytic), called histocytres when entering tissue spaces
Dysfunction Immune Response when immune components are inactive or remain active after effects are beneficial
Function of Antibodies neutralization of bacterial toxins and viruses by: agglutination of antigens, opsonization of bacteria, activation of inflammatory process
Agglutination of Antigen getting rid of antigen by coding/clumping, one antibody acts as a cross link between 2 antigens causing them to bind/clump together
Opsonization of Bacteria antibody-antigen molecule is coded with a sticky substance
Activation of Inflammatory Processes promotes release of vasoactive substances which immobilize other components against invaders
Compliment System small fragments of circulating plasma proteins made in liver, activated when antibody connects with antigen
Requirements for Organism Destruction activation of complement, attraction of macrophages, arrival of killer T-cells
Functions of Compliment System defend against bacterial infection, bridge between natural and acquired immunity, dispose immune complex and byproducts associated with inflammation.
Pathways That Activate Compliment Cascade classic, lectin, alternative
Classic Pathway triggered after antibodies bind to microbe antigens (part of adaptive immunity-humoral)
Lectin Pathway Triggered when plasma protein binds to terminal mannose residue of surface glycoproteins of microbes
Alternative Pathway triggered when complement proteins are activated on microbial surfaces (part of natural immunity)
Complement basically coats antigen with substance that makes them more appealing to neutrophils and other WBCs
Immunomodulators called biologic response modifiers, affects host via direct/indirect effects on components of immunoregulatory network, enhances host immune response (may be therapeutic). Two types: interferons and colony stimulating factors
Interferon (cytokines) nonspecific, protein produced by body, attacks virus. Activates other parts of immune system, has antiviral & anti-tumor qualities. Produced by t cells, b cells & macrophages in response to antigens. SUPPRESSES ANTIBODY PRODUCTION & CELLULAR IMMUNITY
Colony Stimulating Factor (CSF) naturally occurring glycoprotein cytokines, regulates production differentiation activation & survival of hematopoetic cells.
Erythropoetin stimulates RBC production
Thrombopoetin plays key role in development of bone marrow cells
WBC and Differential provides info on type of infection and body's response to it, listed as %
Culture & Sensitivity urine, blood, sputum, wound, abscess, or peritoneal. Helps identifying effect antibacterial drug
Erythrocyte Sedimentation Rate (ESR) rate RBCs settle out of plasma (normal 15-20mm/hr), increased with inflammation or infection
Immunoglobulin Electrophoresis determines presence & quality of specific immunoglobulins (IgA), used to detect hypersensitivity disorders, autoimmune disorders, immunodeficiencies, chronic viral infection, MM, uterine infection
Antibody Screening Test detect presence of antibodies against virus, bacteria, fungi. (+) indicates exposure and development of antibodies to specific antigen
Auto-Antibody Screening Test detects presence of antibodies against persons own DNA (self-cells), associated with RA, SLE, etc
Antigen Tests detect presence of specific antigen (HIV), certain infections/disorders
Gallium Scan nuclear scan, uses radioactive substances to identify WBC hot spots in body, solution accumulates where inflammation present
Warning Signs of Primary Immunodeficiency >8 ear infections yearly, >2 serious sinus infections yearly, >2 months using antibx with little/no effect, >2 pneumonias yearly, failure to gain weight/grow normally (infant), recurrent deep skin/organ abscess, persistent thrush after age 1
Wiskott-Aldrich Syndrome (WAS) genetic, poor prognosis, overwhelming fatal infections, frequent infections, thrombocytopenia, small platelets, increased autoimmune disorder, malignancies. Common S&S: vasculitis, autoimmune hemolytic anemia. RN care: immunosuppression, infection control
Hereditary Angioneurotic Edema deficiency of C1 esterase inhibitor, opposes release of inflammatory mediators, progresses to severe. S&S: recurrent edema in subq tissue, GI tract, & upper airway, hormone fluctuations precipitate it. Tx: fresh frozen plasma
Paroxysmal Nocturnal Hemoglobinuria acquired clonal stem cell disorder, S&S mild to life threatening, increased hemoglobinuria during sleep, can result in aplastic bone marrow
Most Common Transplanted Organ Heart, kidney, liver, lung, pancreas, intestine
Human Leukocyte/Histocompatibility Antigen responsible for rejection of genetically disparate tissues
Sensitization Stage t cell receptors recognize allo-antigens on foreign graft cells->use direct/indirect pathways, NKA cells and other mechanisms to cause apoptosis of cells in foreign graft/organ
Humoral Rejection form of allograft injury/dysfunction primarily mediated by antibody and complement. Can occur immediately or during forst week post transplant.
Dx Test for Transplant Tolearation ABO blood group testing (incompatibility between blood groups leads to rapid rejection), lympho-cytotoxicity assay (tested for reactivity with donor lymphocytes, should be negative)
cyclosporin (Neoral) Action immune suppression by inhibiting t cell to suppressimmune components, supresses b&t cells
cyclosporin (Neoral) Uses prevention & TX of organ rejection, graft v. host disease in bone marrow transplant, autoimmune disorders (RA, SLE, Myasthenia gravis). Given oral, IV for acute rejection. Titrate upward slowly
cyclosporin (Neoral) Side Effects teratogenic, nephro, neuro, hepato toxicity, bleeding gums, fluid retention, hair growth, tremors, seizures, HTN, thromboembolism,
cyclosporin (Neoral) RN Interventions monitor BP, creatinine, liver fx, I&O every 2 weeks until stable, admin first oral dose with milk/OJ over 2-6 hours, stay with patient for first 30 minutes, lifelong therapy, report signs of rejection
azathioprine (Imuran) Action inhibits purine synthesis, inhibits b and t cells and non-immune cells
azathioprine (Imuran) Usage prevents organ rejection, route: PO/IV
azathioprine (Imuran) Side Effects teratogenesis, GI distress, bone marrow depression, increased risk for infections, fever, sore throat, mild leukopenia
azathioprine (imuran) RN interventions monitor labs for neutropenia & thrombocytopenia, interacts with allopurinol, instruct to reports signs of rejection, need for lifelong therapy
cyclosphosphanide (Cytoxan) Action inhibits b cells more than t cells may also attack immuno-competent lymphocytes to inhibit established immune responses
cyclosphosphanide (Cytoxan) Uses immunosuppressant autoimmune blood disorders, severe RA, Wegener's granulomatosis. Given PO
cyclosphosphanide (Cytoxan) Side Effects hair loss, GI distress, bone marrow depression, hemorrhagic cystitis of bladder
cyclosphosphanide (Cytoxan) RN Interventions encourage drinking fluids & voiding often to prevent cystitis
Created by: xwins01