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wvc immune
wvc immune G Mcgregor summer 2011
| Question | Answer |
|---|---|
| HIV Category A- | Manifestations may not be present at this stage, or the person may have persistently enlarged lymph nodes (lymphadenopathy). He or she may have acute but temporary “flu-like” symptoms as the only disease manifestations. |
| HIV Category B- | Bacterial endocarditis, meningitis, pneumonia, or sepsis; Vulvovaginal candidiasis; thrush; Severe cervical dysplasia or carcinoma; fever lasting longer than 1 month; Oral hairy leukoplakia; |
| HIV Category C-wasting syndrome; Bronchial, tracheal, pulmonary, or esophageal candidiasis; Invasive cervical cancer; Disseminated or extrapulmonary coccidioidomycosis; Chronic intestinal cryptosporidiosis; | Cytomegalovirus disease other than that of the liver, spleen, or lymph nodes; HIV-related encephalopathy; Herpes simplex ( bronchitis, pneumonitis; or esophagitis); Kaposi's sarcoma |
| What determines how quickly the HIV infection progresses? depends on how HIV was acquired, personal factors, and interventions. For people who have been transfused with HIV-contaminated blood, for example, AIDS develops quickly. | For those who become HIV positive as a result of a single sexual encounter, the period is much longer before progression to AIDS |
| Etiology of AIDS infection- | Currently in the United States, almost 1 million cases of HIV/AIDS have been diagnosed, and more than 550,000 people have died of AIDS. 40-60 million worldwide have aids/ 30 million have died |
| Retrovirus- | A retrovirus is an RNA virus that is duplicated in a host cell using the reverse transcriptase enzyme to produce DNA from its RNA genome |
| Results of HIV infection on cells are: | Effects of HIV infection are related to the new genetic instructions that now direct CD4+ T-cells to change their role in immune system defenses. The new role is to be an “HIV factory.” |
| Clinical manifestations of HIV- | first manifestations are fever, night sweats, chills, headache, & muscle aches. All of these problems can be caused by exposure to almost any virus, such as influenza—not just to HIV |
| Opportunistic infections - | caused by organisms that are present as part of the normal environment & are kept in check by normal immune function. They occur b/c profound immune suppression of the person w/ AIDS. |
| A diagnosis of AIDS requires that the person be | HIV positive and have either a CD4+ T-cell count of less than 200 cells/mm3 or an opportunistic infection |
| HIV/AIDS related Malignancies- | Kaposi's sarcoma; Non-Hodgkin's lymphoma; Hodgkin's lymphoma; Invasive cervical carcinoma |
| Laboratory diagnostics- | Patients with AIDS are often leukopenic, with a WBC count of less than 3500 cells/mm3 |
| Lymphocyte counts | , patients with HIV/AIDS are often lymphopenic (<1500 lymphocytes/mm3). |
| CD4/CD8 counts | CD4+/CD8+ ratio <2; CD4+ count <200/mm3 |
| Anthrax - | spread by inhalation of spores; vesicular lesions, eschar, edema, ulceration, and sloughing. URI symptoms in the inhaled presentation. Standard precautions unless patient presents right after exposure. |
| Botulism - | toxin ingestion results in dysphasia, dry mouth, drooping eyelids, and blurred or double vision. Vomiting and constipation or diarrhea may be present initially, extending to symmetric flaccid paralysis in an alert person. |
| Lymphatic Plague- | 2-8 days after bites from fleas of an infected rodent (rarely after infected tissue or body fluid contact), onset of fever and chills, painful lymphadenopathy, headache, GI symptoms, & rapidly progressive weakness. 50%-60% fatality if untreated. |
| Pneumonic plauge: | 1-3 days after aerosolized organism inhalation, fever & chills, productive cough, hemoptysis, rapidly progressive weakness. GI symptoms & bronchopneumonia. Survival unlikely if not treated within 18 hr. |
| Smallpox- 10-17 days after droplet or airborne virus inhalation or contact with bleeding lesions, onset of severe myalgias, headache, and high fever. 2-3 days later, a papular rash appears on face and spreads to extremities (and palms and soles). | quickly becomes vesicular, painful & pustular . Patients are infectious at onset of rash until scabs separate (3 wk). May be confused with varicella. |
| The Lymph System & Immunity- | Responsible for returning tissue fluid to the blood and protecting the body against foreign material. |
| interventions for Hyperthermia?- | address the cause of the fever, medicate, external cooling |
| interventions for Dehydration?- | patients require additional fluids either orally or IV. Monitor carefully for signs of dehydration |
| Effective antimicrobial therapy has four requirements. What are they? | correct drug, sufficient dosage, correct route of administration, sufficient duration of administration |
| Inactivation-neutralization- | is the process of making an antigen harmless w/out destroying it. only a small area of the antigen causes the harmful effects. When an antibody binds & only covers up the antigen's active site. |
| Lymphocyte-Function-: | cells mature in the secondary lymph tissue of the thymus and are primarily involved cell mediated immunity. Helper T; suppressor T; cytotoxic T & natural killer cells. |
| Helper/Inducer T-cells function- | 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. (a call to arms) |
| Suppressor T-cells-Function- | prevent hypersensitivity when a person is exposed to non-self cells or proteins. Important in preventing the formation of antibodies directed against normal, healthy self cells, (basis for many autoimmune diseases ) |
| Cytotoxic/Cytolytic T-cells-Function- | destroy cells that contain a processed antigen's major histocompatibility complex (MHC). This activity is most effective against self cells infected by parasites, such as viruses or protozoa. |
| Natural Killer Cells-Function- | have direct cytotoxic effects on some non-self cells without first being sensitized. The cell killing actions of NK cells are independent of the interactions of other white blood cells. |
| What are cytokines? | act like “messengers” that tell specific cells how and when to respond. The cells that change their activity when a cytokine is present are “responder” cells. |
| Hyperacute rejection- | begins immediately on transplantation and is an antibody-mediated response. Antigen-antibody complexes form in the blood vessels of the transplanted organ. |
| Acute rejection- | AMI and CMI cells attack the new organ |
| Chronic rejection- | The smooth muscles of blood vessels overgrow and occlude the vessels. The donated organ tissues are replaced with fibrotic, scarlike tissue |
| Rejection of transplanted solid organs | involves all three components of immunity, although cell-mediated immune (CMI) responses contribute the most to the rejection process. |
| Maintenance Drug Therapy for transplants -combinations of specific immunosuppressants | (cyclosporine); less specific immunosuppressants (azathioprine [Imuran] or mycophenolate [CellCept, Myfortic]); and one of the corticosteroids, such as prednisone |
| Rescue Drug Therapy in Transplants- | Antilymphocyte globulin (ALG) is an antibody produced in an animal after the animal has been exposed to human lymphocytes. Muromonab-CD3 (OKT3) is an antibody directed against the human T-cell cell-surface antigen CD3. |
| Describe some normal defensive systems that prevent introduction of infection into the body: | Intact skin; saliva; mucus, normal flora and natural chemicals. |
| how the body differentiates self from non-self cells: | Human leukocyte antigens are on the plasma membranes of cells, immune cells constantly search out self from non-self in the body. |
| The cells of the immune system originate in the | bone marrow |
| What is a stem cell? | immature undifferentiated cells that will mature into certain cells in response to chemical signals. The body signals to the stem cells the type of cells needed. |
| White blood cells are also called leukocytes and are cells that have what actions? (5) | recognition of self; destruction of invaders, cell debris, unhealthy cells; production of antibodies; complement activation; production of cytokines |
| Which WBC type is involved in the following: Inflammation: | neutrophil; macrophage; monocyte; eosinophil; basophil |
| Which WBC type is involved in the following: | Antibody-mediated immunity: B –lymphocyte; plasma cell; memory cell |
| Which WBC type is involved in the following: Cell-mediated immunity: | T lymphocyte helper/inducer cell; cytotoxic/ cytolitic T- Cell; Natural Killer Cell |
| Neutrophils: Origin & Function- | bone marrow and they destroy invaders by phagocytosis |
| Macrophages: Origin& Function- | bone marrow stimulate long lasting response in antibody mediated immunity and cell mediated immunity. |
| basophils:Origin & Function- | (bone marrow) have granules containing vasoactive amines that act on blood vessels.( histamine, serotonin, kinins, and leukotrienes) |
| What are the actions of the following Heparin- | . Heparin inhibits blood and protein clotting. |
| What are the actions of the following Histamine- | Histamine constricts small veins and respiratory smooth muscles. |
| What are the actions of the following Kinins- | Kinins dilate arterioles and increase capillary permeability. These actions cause blood plasma to leak into the interstitial space (vascular leak syndrome). |
| Leukotrienes- | is to trigger contractions in the smooth muscles lining the trachea; their overproduction is a major cause of inflammation in asthma and allergic rhinitis. |
| Eosinophils: | Origin-& Function- act against infestations of parasitic larvae. Their granules contain some substances that induce inflammation when released. eosinophils degrade the vasoactive chemicals released by other leukocytes. |
| B-lymphocytes:Origin-& Actions (AMI)- | to become sensitized to a specific foreign antigen & to produce antibodies directed specifically against that antigen. The antibody causes one of several actions to neutralize, eliminate, or destroy that antigen. |
| The body learns to make enough of any specific antibody to provide long-lasting immunity and protection against specific organisms or toxins. Seven steps are needed to produce a specific antibody directed against a specific antigen | (invasion), antigen recognition, lymphocyte sensitization, antibody production and release, antigen-antibody binding, antibody-binding reactions, and sustained immunity, or memory |
| Complement fixation- | A system of marking a pathogen for latter destruction by immune cells |
| Precipitation | is similar to agglutination with a larger response. antibody molecules bind so much antigen that large, insoluble, antigen-antibody complexes are formed. These complexes cannot stay in suspension in the blood. |
| Defense Against Disease: Normal or Nonspecific defenses -The first line of defense (3) | Inflammation; Antibody-mediated Immunity; Cell-mediated immunity |
| Nonspecific Defenses….Intact Skin; Mucous membranes; Respiratory tract- cough, lyosome; | Gastrointestinal tract- acidic, normal bowel flora, peristalsis; Genitourinary tract- acidic, flushing action of urine; Recognition of non-self; Inflammation; Antibody-mediated immunity; Cell-mediated immunity |
| Immunine function is most effective with which age group?> | 20-30 years |
| Three parts of the immune system | Inflammation; cell mediated immunity ; anti body mediated immunity |
| Self-tolerance | is the body’s ability to differentiate self or normal cells from invading or non-self organisms; Proteins of each person are unique and serve as an identifier for that person |
| Human Leukocyte Antigens (HLA) are | genetic and specific to that person Cells not recognized as self will initiate action by the immune system. Identifying Proteins that protrude from membrane. |
| The Immune System | Not confined to one organ or area of the body; Most cells of the immune system originate in the bone marrow; spleen and thymus also play a role in immune development. |
| Leukocytes | are the immune system cells, also known as White Blood Cells (WBC) |
| Stem Cells | Immature, undifferentiated cells (What it becomes depends on body needs and presence of certain hormones) Stem cells exposed to a certain hormone will mature into that type of blood cell |
| Inflammation (Nonspecific body defense but can be initiated quickly) | Short-term protection; How widespread the inflammation depends on intensity, severity, duration & extent of exposure |
| Inflammation does not always mean an infection is present | trauma can cause inflammation without infection |
| Results of inflammation (3) | vasodilatation (to get more blood to area); capillary permeability (allows WBC/ proteins through to aid in healing) clotting (seals off area of injury and stops bleeding) |
| Leukocytes: (THE cells of the inflammatory and immune responses) (Three main types): | Granulocytes, monocytes and lymphocytes; Originate from either bone marrow (myeloid) or lymph nodes (lymphoid) |
| Myeloid: | granulocytes & monocytes (originating from the marrow) |
| Lymphoid: | lymphocytes, both B-type and T-type (originating from the lymphnodes) |
| Functions of WBCs Recognition of self versus non-self; Phagocytic destruction of foreign invaders; Lytic destruction of foreign invaders; production of specific antibodies; | Production of hormones that stimulate increased formation of leukocytes; Production of hormones that increase specific leukocyte production |
| Table 19-1 page 309 | |
| Neutrophils - | 55-70% of WBCs, type of granulocytes, segs, polys, bands… arise from bone marrow, 12-18hr lifespan; when mature classed as segs & polys…immature cells called bands or stabs |
| Left shift | more immature neutrophils cells are being released due to the pressure of infection. If the number of immature cells increases, the body is unable to keep up with the infection |
| Segs | only type of neutrophil effective in phagocytosis (mature neutrophil) |
| Macrophages- | Distinguish self from non-self, stimulate AMI and CMI, phagocytosis, repair injured tissue, release of cytokines, highly concentrated in GI tract, liver and spleen. |
| Monocytes | are less mature machrophage |
| Kupffer | fixed macrophage in liver to filter poisons |
| Histocytes & dendredgic cells | machorphages |
| Basophils- | Rarest type, contain chemicals that act on blood vessel walls and smooth muscle (vaso-active); release of vaso active amines |
| Eosinophils- | 1-2% of WBCs, Control or modulate the inflammatory reaction ( will be elevated during an inflammatory response); also in parasitic infection) controls vaso-active chemicals |
| Mast cells – | Granulocyte cells that activate the inflammatory response. (mast cell stabilizer will reduce the activation of inflammation) |
| Macrophages | Distinguish self from non-self; Stimulate antibody-mediated immunity and cell mediated immunity; Involved in phagocytosis, repair of injured tissue, antigen processing and cytokine secretion. |
| Neutrophils (Make up 55%-70% of WBCs) | Mature in 12 to 14 days; Life span of 12 to 18 hours; Mature neutrophils are segs or polys; Less mature cells are bands or stabs; |
| Eosinophils (Make up 1% to 2% of WBCs) | Control or modulate the inflammatory process; Not efficient at phagocytosis; Will be elevated in allergic reactions or parasitic infestations |
| Basophils (Rarest type of leukocyte) | Contain chemicals that act on blood vessel walls; Cause the symptoms of inflammation; Release vasoactive amines (heparin, serotonin, kinins, & leukotrines) |
| Mast Cells (Probably the most important activator of the inflammatory response) | Develop in the bone marrow and stored in the loose connective tissue near the blood vessels) Activate the inflammatory response by: Phagocytosis, Degranulation and Synthesis |
| Degranulation (mast cells) – | release preformed granular contents into the extracellular tissue; |
| Synthesis (mast cells)– | synthesizes certain mediators in response to stimulus, such as cytokines; |
| Steps of phagocytosis | Exposure; attraction; adherence; recognition; cellular ingestion; phagasome formation; degradation. |
| Stages of Inflammatory Response Stage I - | Vascular, brief vasoconstriction at site in response to trauma >> followed by hyperemia and edema formation. redness, warmth, dilutes concentration of toxin |
| Stages of Inflammatory Response Stage II- | Cellular exudate. Increased neutrophil production and formation of exudate, |
| Stages of Inflammatory Response Stage III- | Tissue repair and replacement. Healthy tissue is stimulated to divide, increased blood vessel growth &nscar formation; fights infection but does not provide immunity. |
| Story of a Splinter | Splinter penetrates intact skin; Recognized as non-self; Initial vasocontriction and pain at the site then hyperemia; Increased neutrophils form exudate; Skin barrier is repaired |
| True or false ---Response is the same weather the insult to the body is a burn or otis media or soft tissue injury or abscess? | True |
| Which cells participate in phagocytosis | macrophages & neutrophils |
| The body produces the most of what type of wbc | neutrophil |
| Innate or Native Immunity | Genetically determined; Cannot be developed or transferred from one person to another; Is not an adaptive response to exposure; Nonspecific & encompasses inflammatory responses |
| Natural Immunity Active- | After exposure to an antigen, the body makes antibodies specific to that antigen |
| Natural Immunity Passive- | Antibodies are passed from one person to another, like mother to fetus or infant |
| Artificial Immunity Active (making your own)- | Small amounts of specific antigen are injected into the body, the body responds by making antibodies…most vaccines are this type. Tdap/ MMR/; long lasting w/ boosters (tetnus vac) |
| Artificial Immunity Passive (getting them from a outside source) - | Injecting antibodies produced by another person or animal. Serious disease where there would be no natural immunity. Snakebite or rabies (tetnus toxin) |
| Antibody-Mediated Immunity (Also called humoral immunity) | Involves Antigen-Antibody interactions; Antibodies are produced by B-lymphocytes |
| Antibodies | neutralize, eliminate or destroy specific antigens; For effective AMI to occur, the entire immune system must function adequately |
| Main cells in the antibody mediated Immunity | mostly b cells and some t-cells |
| B cells divide into | memory cells(for latter use) and plasma cells (to produce antibodies now) |
| Seven Steps of Antigen- Antibody Interaction | Exposure & Invasion >Antigen Recognition> Lymphocyte Sensitization> Antibody Production & Release> Antigen-Antibody Binding> Antibody-Binding reactions> Sustained Immunity: Memory |
| Seven Steps of Antigen-Antibody Interaction Exposure & Invasion (Step 1) | Antigen enters the body; Enough antigen must invade that it overwhelms the body’s inflammatory response; There may be an incubation period while the disease develops enough antigen |
| Seven Steps of Antigen-Antibody Interaction Antigen Recognition (Step 2) | Unsensitized B-lymphocytes recognize the antigen as non-self; Cooperative effort of B-lymphocytes, macrophages and T-cells |
| Seven Steps of Antigen-Antibody Interaction Lymphocyte Sensitization (Step 3)(B-lymphocyte recognizes antigen as non-self) | B-lymphocyte becomes sensitized to this antigen, each cell can only become sensitized to one antigen. Sensitized B-lymphocyte divides into two: plasma cell and memory cell |
| Seven Steps of Antigen-Antibody Interaction Antibody Production & Release (Step4) (Antibodies are produced by the plasma cell.) | Plasma cells can produce 300 molecules of antibody /sec. Antibodies are specific to the antigen that stimulated their production; Antibody molecules are secreted in the blood & ECF (they now have humoral immunity) |
| Seven Steps of Antigen-Antibody Interaction Antigen-Antibody Binding (Step 5) | Antibody is a Y-shaped molecule; Can bind to 2 antigen molecules or 2 sites on an antigen; Binding the antigen starts other actions that cause its destruction |
| Seven Steps of Antigen- Antibody Interaction- Antibody-Binding reactions (Step 6) | antigen is neutralized or marked by the antibody |
| Seven Steps of Antigen- Antibody Interaction: Sustained Immunity: Memory (Step 7) | memory cells remain ready to react to antigen if it were to reappear in the future, as a result future attacks will be resolved more quickly |
| Accglutination | the clumping together of larger complexes of antibody and antigen complexes |
| Complement system | marks surface of invaders to bring wbc to the invader for destruction |
| Sustained Immunity | Memory cells made during sensitization of the B-lymphocyte Remain sensitized to the specific antigen; Re-exposure to that antigen causes memory cells to respond quickly with increased antibodies |
| Cell-Mediated Immunity (Produced by lymphocyte cells that mature in secondary lymphoid tissues in the thymus and pericortical areas of lymph nodes) | T-lymphocytes and Natural Killer Cells; CMI responses influence and regulate inflammation and antibody-mediated immunity via cytokines. |
| Cell-Mediated Immunity Cells are (4) | Helper/Inducer T-cells; Suppressor T-cells; Cytotoxic/Cytolytic T-cells; Natural Killer Cells (Important in preventing cancer & metastasis) |
| Cytokine Cascade (Cytokines are small protein hormones produced by the leukocytes and some other tissues) | Cytokines bind to receptor cells & change its activity; Cytokines include interleukins, interferons, colony stimulating factors & TNF; The cytokines can have specific actions but can also stimulate widespread reactions, many of which are pro-inflammatory |
| Helper/Inducer T-cells (Also called T4 cells or CD4+ cells) | Recognize self versus non-self; Stimulate the activity of other leukocytes in the presence of antigens; Act as organizers or “call to arms” defensive action |
| Suppressor T-cells (Also called T8 or CD8 cells) | Prevent overreactions to non-self cells; Prevents the formation of auto-bodies against normal healthy self cells; Opposite action of T4 cells/ prevent over reaction & auto immune |
| Helper t and suppressor t cells work to? | keep each other in balance to prevent over or under reaction |
| Cytotoxic/Cytolytic T-cells (Also called Tc cells) | Destroy cells that contain MHC found in parasitic organisms, viruses, protozoa; Makes holes in the membrane of the infected cells and delivers a “lethal hit” of enzymes |
| Natural Killer Cells(Also called NK cells) | Not a true T-cell; Delivers direct cytotoxic effects on non-self cells; Conducts “seek & destroy” missions to eliminate invaders and unhealthy self cells..viral & cancer cells |
| Which cells start the antibody production in the presence of an invader? | Macrophages, T-helper, b-lymphocytes |
| Virulence | how easily I disease is communicated and how invasive it is |
| Pathogenicity | the ability to cause disease |
| Coliziation | pathogen present in the tissue, but not causing symptoms of infection…colonization does not mean they have the disease or they are infected. |
| Sub clinical | The person has the disease but they are not present symptoms as of yet. Early stages but may not be showing symptoms |
| Portal of Entry (Where microorganisms enter the host) | Respiratory Tract; Gastrointestinal Tract; Genitourinary Tract; Skin or Mucous Membranes; Blood |
| Mode of Transmission | (How organisms are spread from one host to another) |
| Direct contact- | The source and host have physical contact; skin to skin or mucous membrane to mucous membrane; |
| Indirect contact- | Transfer from one host to another via a fomite, droplet spread or ingestion of pathogen |
| Airborne Transmission | Small, airborne particles leave infected source and travel as droplet or dust; Colds, TB, Influenza, measles, meningitis, chickenpox are examples of organisms that travel this way |
| Vehicle Transmission | Infectious agents are transmitted through a common source; Contaminated food, water; Typhoid, salmonella, cholera |
| Vectoborne Transmission | Involves insects or animals as a means of transmitting the pathogen; Ticks or mosquitoes can spread disease through their bites; Flies can carry organisms from one place to another |
| Portal of Exit | Infectious organism leaves one host who has become a reservoir for infection; Most often exits through the same door as it entered; Sometimes can exit through several routes (chickenpox) |
| Infection Control…. Break the chain of infection: handwashing, good hygiene, sanitation, sterilization and barriers; Improve immune defenses; Immunity; | Improved Response; Adequate sleep & rest; Prolactin, estrogen; Growth hormone; Vitamin D; Good nutrition – fruits, vegetables, fatty acids, proteins; Alternative med- licorice, garlic, ginseng, honey |
| Factors that contribute to Decreased immune response | Stress; Testosterone; Lack of Vitamin C; Obesity; Malnutrition |
| Standard Precautions | recognize all body fluids are potentially infectious and protect ourselves accordingly. |
| Contact Precautions | private room or cohort; gloves; gown; wash hands; dedicate equipment; C-diff; MERSA in wound; Ebola; lice; scabies; |
| Droplet Precautions | large enough molecules will fall to ground within 3 ft; private room; gown; gloves, mask within 3 ft; MERSA in lungs; diphtheria; mumps; strep; meningtius; |
| Airborne Precautions | most careful precaution, negative pressure room; filter; immunity to disese; transport for essential reasons only; TB, chicken pox (occasionally), disseminated shingles; rubella; |
| Laboratory Diagnostics Identify the organism - | C& S; CBC- elevation in leukocytes and differential of types of leukocytes ESR-Sedimentation rate of erythrocytes. Elevated in acute phase inflammation and in chronic inflammatory disease |
| Radiographic Diagnostic | Look at the activity or destruction by an infectious organism ( CXR, Sinus films, joint, GI studies, renal films, CT, MRI, Ultrasound and use of radioactive isotopes, Biopsy of tissue for pathology) |
| Fever Control | Antipyretic drugs - Aspirin, Acetaminophen, Ibuprofen; External cooling; Fluid administration-either oral or IV |
| Antimicrobial Therapy(Antibiotic, antivirals and antifungals) | Four requirements for effective drug treatment: correct drug, sufficient dosage, correct route of administration, sufficient duration of administration |
| Penicillin, Cephalosporins- | inhibit cell wall sythesis |
| Antifungals- | injure the cytoplasmic membrane |
| Erythromycin, Tetracycline and Gentamycin- | inhibit biosynthesis and reproduction |
| Actinomycin- | inhibits nucleic acid synthesis |
| Antibiotic Allergy | Most antibiotics have some side effects, mainly GI, Symptoms of allergy include: Flushing, wheezing, sneezing, pruritis, urticaria, rashes; Anaphylaxis can cause death |
| Impaired immune and Hemapoietic function | Cancer destroys normal tissue; Tumor cells enter bone marrow & cause decreased production of normal WBCs; It decreases the number of RBCs & platelets; person becomes anemic & has increased tendency to bleed |
| Altered Nutrition | person w/ cancer often becomes anorexic/ Poor nutrition impacts immune system making the person immunocompromised; Cancer treatment can cause N&V to further exacerbate the problem |
| Cancer Prevention | Avoid known carcinogens; Cancer screening for early detection; Chemoprevention- involves the use of exogenous chemicals found in plants and other sources to disrupt at least one step in cancer development |
| Benign cell growth | growth is harmless and does not require intervention Malignant cell growth is serious and can be life-threatening |
| Characteristics of Normal Cells | Have limited cell division; Show specific morphology; Have a small nuclear-cytoplasmic ratio; Perform specific differentiated functions; Adhere tightly together; nonmigratory; Grow in orderly/ well-regulated manner; contact inhibited |
| Characteristics of Embryonic Cells (stem cells) | Rapid, continuous cell division; Anaplastic morphology; Large nuclear-cytoplasmic ratio; No differentiated functions; Adhere loosely together; Migratory; Not contact inhibited |
| Characteristics of Benign Cells | Continuous or inappropriate cell growth; Specific morphology; Small nuclear-cytoplasmic ratio; Performs differentiated functions; Adhere tightly together; Nonmigratory; Grow in an orderly manner |
| Characteristics of Malignant Cells | Rapid or continuous cell division; Anaplastic morphology; Large nuclear-cytoplasmic ratio; Lose some or all differentiated function; Adhere loosely together; Able to migrate; Grow by invasion; Not contact inhibited |
| Cancer Development | Carcinogenesis or oncogenesis (development of cancer); As a cell changes from normal appearance to malignant it is called malignant transformation; 4 steps to cancer development: initiation, promotion, progression & metastasis |
| Causes of Cancer Development- | 3 factors influence development of cancer: Environmental exposure to carcinogens, genetic predisposition and immune function; Activation of proto-oncogenes (early embryonic genes) into Oncogenes; |
| Immune System & Cancer.. immune system protects the body from non-self cells; Non-self cells include those that are no longer normal, such as cancer cells; Cell-mediated immunity is the part of the immune system that is responsible for cancer protection; | Natural Killer & Helper T-cells are surveillance cells that detect cancer cells & initiate response; Things which affect the immune system also influence the development of cancer |
| Maintenance- used for routine immunosuppressive therapy. (Anti-rejection Drugs)Combinations of specific and less specific immunosuppressives & corticosteroids--- | reduce immunologic responses during rejection episodes. May be used in addition to or in replacement of maintenance drugs post-transplantation |
| Autoimmunity-An inappropriate immune response against normal, healthy self-cells by antibodies or lymphocytes…Cause is uncertain | Autoimmune antibodies have been detected in a number of diseases: SLE, RA, Scleroderma, Hashimoto’s thyroiditis and diabetes type I. Sjogren’s and Goodpasture’s syndrome are both considered autoimmune disorders |
| Goodpasture’s syndrome | antibodies made against glomerlus also effects the lungs. Sx. foamy, bloody, or dark colored urine, decreased urine output, cough w/ bloody sputum, difficulty breathing after exertion, weakness, fatigue, n&V, |
| Sjogren’s syndrome | sjögren’s syndrome is a chronic autoimmune disease in which people’s white blood cells attack their moisture-producing glands |
| Rheumatoid Arthritis | Autoimmune response that causes inflammation of the joints, particularly the synovial membrane; Prolonged inflammation damages the cartilage and the bone, if left unchecked. |
| Rheumatoid Arthritis Diagnostics include Rose- | Waaler test, ANA titer and ESR |
| Rheumatoid Arthritis Treated with | NSAIDS, Steroids, immune suspressive drugs like sulfasalazine |
| Systemic Lupus Erythematosus (SLE) | Autoimmune disorder that is systemic and involves connective tissue, characterized by exacerbations and remissions; 8-10x more common in women, vasculitis w/in organs & tissues, interferes w/ O2 carrying ability of vessels |
| Diagnostics for SLE include: | ANA titer, ESR, more specific tests SSA, SSB and AP monitor antibodies that are associated with SLE; TX: includes glucocortocoids, Plaquenil, Cytoxan. Leading cause of death is kidney failure |
| Altered Cell Growth…cells and tissues is normal during childhood but some growth stops when development is complete; | Some cells continue to grow in areas where wear and tear makes it necessary to replace damaged cells Benign cell growth is harmless and does not require intervention Malignant cell growth is serious and can be life-threatening |
| Type III Hypersensitivity: Immune Complex Reactions | Soluble immune complexes are formed with antigen excess; These are deposited in the walls of small blood vessels; Complement cascade is activated resulting in tissue and vessel damage. RA/ SLE/ serum sickness/ |
| Type IV Hypersensitivity: Delayed Sensitized T-lymphocytes from a previous exposure respond by producing chemical mediators; They recruit and activate macrophages; | The lymphocytes and macrophages accumulate and cause edema, ischemia and tissue destruction (Examples are PPD, poison ivy rash, local response to insect stings, tissue transplant rejection) |
| Type V Hypersensitivity: Stimulatory Reactions… Inappropriate stimulation of a normal cell surface receptor to an antibody; Results in continuous “turned on” state for the cell; | The tissue responding to the autoantibody is out of control and does not respond to the body’s normal feedback system. Ex. Graves’ disease type of hyperthyroidism (not responding to feedback system) |
| Transplant Rejection | Natural Killer cells and cytotoxic/cytolytic T-cells recognize and destroy cells from other people; Newly transplanted organ is not identical match and is recognized as non-self (Can be hyperacute, acute or chronic) |
| Hyperacute rejection…. Antibody-mediated response; Begins immediately after transplantation; The host body has pre-existing antibodies to one or more antigen in the donor organ; | Blood clotting cascade is initiated and diffuse coagulation takes place; There is massive cellular destruction and loss of the transplanted organ. Most at risk is w/ many transfusions or pregnancies. |
| Acute Rejection….Within 1 week to 3 months after transplant; AMI results in vasculitis within the transplanted organ; | Cytotoxic/cytolytic T-lymphocytes and Natural Killer cells infiltrate the organ cells and cause lysis; If diagnosis can be made and interventions done quickly, the organ can be saved w/ steroids |
| Chronic Rejection…Inflammation and scarring takes place (Scar tissue replaces functional tissue); Long-standing and occurs continuously in response to constant ischemia; | Major cause of death in those who have survived 1 or more years after heart transplant; Probably occurs to some extent in all solid organ transplants |
| Radiation-induced immunodeficiencies- | radiation is cytotoxic to proliferating and resting cells. Lymphocytes are sensitive to radiation. Radiation of large bones can cause general immunosuppression in the primary blood cell producing sites. |
| Hypersensitivity: Allergies | The body overreacts to invaders and antigens, Increased and excessive reaction to an antigen to which the body has previously been exposed (The terms hypersensitivity and allergy are synonymous) |
| Types of Hypersensitivity; | Type I: Immediate; Type II: Cytotoxic; Type III: Immune-complex mediated; Type IV: Delayed; Type V: Stimulated |
| Type I: Immediate Hypersensitivity (AKA atopic allergy) | Most common type; ^ production of IGE; Acute inflammatory response to harmless antigen; Release of histamine & vasoactive amines from the basophils, eosinophils and mast cells. Ex. hayfever, allergic asthma & anaphylaxis |
| Interventions for hypersensitivity | Avoid the allergen or food; Drug therapy. Complementary or alternative therapy; Desensitization therapy |
| Drug Therapy for hypersensitivity | Decongestants; Antihistamines; Corticosteroids; Mast Cell Stabilizers; Leukotrine Antagonists; (Complementary therapy: Desensitization) |
| Anaphylaxis (Extreme Type I reaction) | Systemic; Affects multiple organs in seconds to minutes after exposure to allergen; Life-threatening, feeling of uneasiness, swelling; wheezing; hypotension; cardiac collapse. |
| Latex Allergy (type 1 reaction) | Hypersensitivity to a protein found in natural latex; Contact dermatitis can be a sign of allergic reaction; Increasing incidence, particularly in individuals with high exposure to latex products; Use of latex products in hospitals is decreasing |
| Type II Hypersensitivity: Cytotoxic | Antibodies are made against self-cells and tissues. The self-cells are destroyed by phagocytosis. Goodpasture syndrome, blood reaction |
| Assess support system | may be abandoned by their family & partner may not be able to make health care decisions; Stigma attached to diagnosis; Assess ability of client to comply with treatment plan; Depression may accompany diagnosis |
| HIV antibody test | Enzyme-linked immunosorbent assay & Western blot |
| Normal T-cell count | 600-1500 |
| Drug Therapy for AIDS patients | (drugs work best in cocktail or HAART type regiment); Nucleoside Analog Reverse Transcriptase Inhibitors; Non-nucleoside Analog Reverse Transcriptase Inhibitors; Protease Inhibitors; Ribonucleotide Reductase Inhibitor; Antimicrobials for infections |
| Take drugs as it is prescribed | or it will not work as well d/t drugs effecting the viral replication phase. |
| Care focus for AIDS patients | Minimize infections; Maintain adequate respiratory function; Maintain nutrition; Maintain skin integrity; Assess and identify support system; Maintain quality of life and dignity |
| Nutrition Related Deficiency | Adequate balanced nutrition is necessary for the proper function of the immune system; Protein-calorie malnutrition (PCM) impairs T-lymphocyte production and causes a deficiency in protein synthesis |
| Obesity is associated with decreased action of neutrophils and impaired cell-mediated immunity. | Excess fat has a suppressive action on all aspects of immune function. Obese people can be malnourished. |
| Drug-induced immunodeficiencies | Cytotoxic drugs – chemotherapy interferes with proliferation of cells including WBCs; Corticosteroids-Inhibit inflammation, keep T-cells in the bone marrow and suppress CMI |
| Key Features of AIDS | Include manifestation/symptom in immune, integument, respiratory, GI and CNS, Opportunistic infections, Malignancies |
| Opportunistic Infections | Infections caused by microorganisms that are normally present in the environment but do not pose a threat to a person with a healthy immune system |
| Protozoal Infection opportunistic infection | The most common opportunistic infection in clients infected with HIV is Pneumocystitis jerivicci pneumonia 75%-80% of clients with AIDS |
| Toxoplasmosis encephalitis | opportunistic infection in AIDS pts. caused by toxoplasma gondii found in cat feces and undercooked meat |
| Cryptosporidiosis | opportunistic infection causes diarrhea from mild to wasting & electrolyte imbalances, can loose up to 15-20 liters/day |
| Overgrowth of normal flora Candida albicans | opportunistic infection: Candidiasis may occur in mouth, esophagus or vagina |
| Bacterial Infections:The most common bacterial infection in AIDS is | Mycobacterium avium-incellulare complex (MAC); Can be in the respiratory or GI tract; Tuberculosis occurs in 2% to 10% of AIDS pts;Recurrent pneumonia from bacterial infections is common among immunocompromised clients |
| Viral Infections in AIDS patients | Cytomegalovirus (CMV) can infect multiple body systems; Herpes Simplex virus can be site specific or systemic; Varicella zoster virus recurs as shingles in clients w/ history of chickenpox |
| Malignancies in AIDS patients | Because T-cells and macrophages are affected by the HIV, the incidence of cancer in these patients is increased. Kaposi’s sarcoma and lymphomas are the most common types associated with HIV infection |
| Kaposi’s sarcoma is often seen as | small, purplish brown lesions anywhere on the skin |
| Neurologic Complications in AIDS patients | AIDS dementia complex (ADC) is a group of signs and symptoms that indicate CNS involvement d/t infection; up to 70% of AIDS patients; Can also have peripheral neuropathies and myopathies |
| MOA of AIDS Virus | Causes destruction of CD4 helper/inducer T-lymphocytes and macrophages, through replication of its own DNA/RNA in the hijacked cells. |
| Percentage of new HIV infections in minorities in the US? | 72% |
| Which group has highest percentage of AIDS cases in North America | men who have sex with other men |
| Basic PEP = | Two drugs: (zidovudine plus lamivudine or emtricitabine); or (stavudine plus lamivudine or emtricitabine); or (tenofovir plus lamivudine or emtricitabine). When PEP therapy is instituted, the recommended course is 28 days |
| Expanded PEP (When PEP therapy is instituted, the recommended course is 28 days)= | Three or more drugs: (zidovudine plus lamivudine or emtricitabine plus lopinavir/ritonavir); or (stavudine plus lamivudine or emtricitabine plus lopinavir/ritonavir); or (tenofovir plus lamivudine or emtricitabine plus lopinavir/ritonavir). |
| Sexual Transmission of HIV | Transmitted easily in highly mucous areas of vagina, rectum and mouth – oral sex, anal sex and vaginal sex with infected person is risky; The higher the viral load or concentration of HIV, the more risky |
| Parenteral Transmission of HIV | IV drug users – teach them to clean their equipment with bleach solution, do not share needles; Hospital workers – Use needle less system, do not recap, dispose of needles properly, Standard precautions |
| HIV Transmission Blood transfusion- | Donated blood is screened for HIV antibodies. Transmission by this route has been reduced to 0.02% |
| HIV Perinatal Transmission | Risk of transmission from infected mom to baby is between 14%-40%; Can be passed across the placenta, during birth exposure to vaginal secretions and blood or through breast milk |
| Pregnant women with HIV were given an antiviral drug | (Retrovir) and had a decreased incidence of passing on the virus – 8.9% versus 25% in those given the placebo |
| Immunodeficiency | Deficient response of the immune system due to a missing or damaged component |
| Primary immunodeficiency | is one that is present from birth |
| Acquired immunodeficiency | is one that occurs as a consequence of injury, disease, exposure to toxins, medical therapy or unknown cause. In either case, the person is said to be immunocompromised |
| Congenital Immunodeficiency born with defect in the development of one or more components of immunity | (Bruton’s Agammaglobulinemia. Common Variable Immunodeficiency (treat with serum immunoglobulin (very expensive), Selective Immunoglobulin A deficiency….does not receive immunoglobuilin treatment) |
| Acquired Immunodeficiency | Acquired Immunodeficiency Syndrome (AIDS); Nutrition-related deficiency |
| Therapy-induced immunodeficiency | Drug induced; Radiation induced |
| Acquired Immunodeficiency Syndrome (AIDS) | AIDS is the late stage of a continuum of syndromes resulting from infection with the Human Immunodeficiency Virus (HIV) |
| A person with HIV infection can transmit the disease to others | at any stage of the disease |
| Categories of HIV infection | Categorized on basis of CD4+ T-lymphocyte count and symptoms |
| HIV/ AIDS Category A – | HIV positive, T-cell count >500 (A1), 200-499 (A2), <200 (A3), asymptomatic, lymphadenopathy |
| HIV/ AIDS Category B – | Illness attributed to or indicative of HIV; complicated by HIV , T-cell count >500 (B1), 200-499 (B2), <200 (BA3) |
| HIV/ AIDSCategory C- | Considered to have AIDS, T-cell count >500 (C1), 200-499 (C2), <200 (C3) |
| AIDS | Profound suppression of immune system due to HIV infection; Type 1 is the form most frequently found in USA, Europe and Asia; Type 2 is endemic to West Africa; Retrovirus causing change in the cell DNA synthesis and rapid replication of HIV |
| MOA of AIDS Virus | Causes destruction of CD4 helper/inducer T-lymphocytes and macrophages, through replication of its own DNA/RNA in the hijacked cells. |
| HI/ AIDS Drug Therapy- How do they work? Most antiviral agents inhibit viral replication and are inactive against latent virus. | Mechanisms for antiviral therapy include interference with viral attachment to the host cell membrane and entry in to the host cell, inhibition of transcription or translation, or interference with viral assembly. |
| Drug-induced immunodeficiency- Describe how each of the following drugs can impair the immune system: Cyclosporine | induces immunosuppression by inhibiting the first phase of T-cell activation (e.g., interleukins, TNF, & interferon) that allow T-cells to progress from the G0 to G1 phases |
| Drug-induced immunodeficiency- Describe how each of the following drugs can impair the immune system: Cytotoxic drugs- | these drugs effect cells that divide most frequently, bone marrow cells are adversely effected by the cytoxic effects of these drugs |
| Describe how the following drugs can impair the immune system: Corticosteroids- | decrease inflammation by inhibiting the release of leukocytic acid hydrolases, preventing macrophage accumulation at the site of infection, |
| ratio of CD4 cells to CD8 cells | This is calculated by dividing the CD4 value by the CD8 value. In healthy people, this ratio is between 0.9 and 1.9, meaning that there are about 1-2 CD4 cells for every CD8 cell. |
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