Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Chronic Exam 4
Exam 4
| Term | Definition |
|---|---|
| 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
Popular Nursing sets