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Self-Def:#2 Immunity
Nursing Patho-Pharm Immune Systems part 2
| Question? | Answer? |
|---|---|
| 3 disorders of the immune system are: | – Hypersensitivity Disorders – Autoimmune Disorders – Immunodeficiency Disease |
| What is An exaggerated immune response to a foreign agent resulting in injury to the host (Non-Self invading the body) Differentiated by the source of the antigen against which the hypersensitivity response is directed | Hypersensitivity |
| Diseases caused by hypersensitivity are characterized by ____ _____ that initiate ______ and result in destruction of _____ tissue | Immune Mechanisms Inflammation destroys healthy tissue |
| List the 5 different types of Allergic/Hypersensitivity Disorders: | Latex Allergy Type 1 - IgE Mediated REactions: Immediate Hypersensitivity Type 2 - Antibody Mediated: Cytotoxic Disorders Type 3 - Immune Complex Disorders: Autoimmune Type 4 - Delayed Cell Mediated |
| What is Characterized by the production of IgE antibodies after exposure to a foreign protein allergen (antigen) Causes the release of inflammatory mediators for sensitized mast cells (IgE is found on the surface of mast cells/Basophils) | Type I – (IgE Mediated Reactions): Immediate Hypersensitivity: Immediate Responses |
| What is from Blood issues and blood is not compatible. Characterized by the formation of antibodies (IgG & IgM) against cell surface antigens Antibody reacts with antigen, activates complement, causing cytolysis or phagocytosis | Type II – Antibody Mediated: Cytotoxic Disorders |
| What is Characterized by the formation of antibodies (IgG, IgM, IgA) that interact with antigens to form antigen-antibody complexes. o These complexes activate complement and cause an inflammatory reaction | Type III – Immune Complex Disorders: Autoimmune Disorders |
| What is mediated by T Lymphocytes NOT antibodies Sensitized T cells react with a specific antigen to induce an inflammatory response | Type IV – Delayed Cell Mediated |
| What is when the cells of the transplant recipient attack the donor cells of the transplanted organ? Involves cell mediated (T) and circulating antibodies (B) that are going to attack foreign invasions. Pt.’s with transplants will be on meds for life. | Host vs. Graft Disease |
| 3 Types of Host v Graft Disease: a. Immediately after transplant a. First few months a. Occurs over a prolonged period of time, characterized by dense fibrosis of organ involved | 1 - Hyperacute 2 - Acute 3 - Chronic |
| What occurs mainly in those who undergo bone marrow transplants? Primary targets include the skin, liver, intestines and cells of immune system Characterized by fever, rash, GI disturbances | Graft Vs Host Disease |
| What are are environmental antigens that cause an atypical exorbitant (in a big way!) immune responses in genetically predisposed individuals – the type of hypersensitivity is type 1 | Allergies |
| Common offenders of Allergies are: | 〉 Pollen, Mold, Grass 〉 Animals 〉 Foods 〉 Cigarette smoke, Dust (mites) |
| Why is someone "allergic?" | - These individuals are thought to produce higher concentration of IgE or have more receptors on mast cells for IgE |
| Treatment: When allergic reaction occurs: Use what in mild reactions b/c symptoms mainly caused by histamine release? Use what in Severe allergic reactions (anaphylaxis)? | Anti-Histamines Epinephrine |
| Allergy Testing looks for & done through: ____ ____ testing or ____ test Looking for ____ & _____ (redness) Diameter of flare = sensitivity to allergen Can also do RIST or RAST testing; means? | Intradermal skin testing or prick test Looking for wheal and flaring (redness) Diameter of flare = sensitivity to allergen Can also do RIST or RAST testing o RIST = radioimmunosorbent o RAST radioallergosorbent |
| What is when the body recognizes “self” as “non-self” & are unsure of trigger o Possibly: Stress, Heredity, Virus, or ↓ Immunity | Auto-Immune Disorders |
| Autoimmune disease affecting all organs Characterized by remissions and exacerbations – goal is to keep pt. in remission & avoid exacerbations which decreases injury to organs. What's the Prognosis? | Systemic Lupus: Prognosis improved with early diagnosis and treatment: Chronic disease, non-curable. Can affect any connective tissue; some pt.’s have problems other don’t |
| 3 Classifications of Lupus are: | 1 - Drug Induced 2 - Discoid Lupus 3 - Systemic Lupus |
| associated with Procan, Apresoline, and some antiepileptic drugs (usually D/C drug, effects will dic)? | Drug-Induced Lupus |
| limited to skin? | Discoid Lupus |
| Most common; involves one or more body systems: kidneys, lungs, musculoskeletal, hematological? | Systemic Lupus |
| Patho of Lupus: Produces _______, specifically against ___, secondary to hyperactive B – cells type? | Auto-Antibodies DNA Type III |
| Patho Lupus cont: These autoantibodies combine with _____ to form ____ _____; and accumulates within connective tissue that triggers inflammatory response There can be destruction of what or damage to the what involved | Antigens Immune Complexes Destruction of connective tissue Damage to the organs involved |
| Main S/S of: General s/s, polyarthralgia, alopecia, pericarditis, pleuritis, Glomerulonephritis, and CNS damage? | LUPUS S/S |
| 5 main treatments for Lupus | NSAIDS Anti-Malarials Corticosteroids Immunosuppressive drugs Cytotoxic Drugs |
| Suppression of lymphocytes proliferation Large doses given to suppress the immune system Uses range from suppression of transplant rejection, to treatment of asthma, & in autoimmune disorders such as: SLE, RA, and erythematosus | Prednisone |
| o One of the most effective immunosuppressants available • Given w/ steroids and following transplants Autoimmune diseases: SLE, RA, psoriasis, myasthenia gravis and DM Type 1 Mechanism Of Action – suppress T lymphocytes’ communication | Cyclosporines |
| - Alternative to Cyclosporine, if lupus has effected kidneys do not give Prograf - More effective, BUT more toxic - Mech. of Action – similar to Cyclosporine - Adverse effects – infection, Nephrotoxicity (33-40%), neurotoxicity, anaphylaxis | Tacrolimus (Prograf) |
| Cytotoxic drugs – given to pts with lupus Toxic to B and T cells that are undergoing proliferation Adverse effects: because they are toxic to all proliferating rapidly cells | Cyclophosphamide & Methotrexate |
| A chronic, progressive, systemic, AU ds w/ inflammation of joints & deformity Onset is insidious and have remissions and exacerbations ⇨ Characterized by: o Chronic Inflammation of bilateral joints and surrounding structures – multiple joints involve | RA: Rheumatoid Arthritis |
| Patho of RA: Exposure to a viral pathogen may initiate the inflam resp; __ is formed & producing autoantibodies against own ___, cell type? What's located within the joint capsule and responsible for producing synovial fluid to lubricate? What happens? | IgG IgG, Type III Synovial Membrane Hypertrophies & thickens secondary to inflammation |
| RA Patho: What is occluded and cellular necrosis occurs? What forms in the synovial membrane: may extend into joint capsule and bone; secondary to underlying ds proc- leads to deformity or from Unknown trigger (viral) initiates inflammatory cascade: | Blood Supply Vascular Granulation Tissue |
| S/S Stages of RA: vague – anorexia, weight loss, fever, loss of energy? nflammatory signs, swelling, decreased movement of joints in the hand, feet, wrists, and elbows? joints of the knees, hips and cervical spine, resulting in permanent joint damage | New Onset Early Disease, As RA progresses End Result = Bone Erosion |
| RA Diagnostic Criteria based on what? | Combination of four criteria |
| Inc RF of RA: Rates increases with increasing age in both genders Incidence rates consistently higher in women with Risk greatest before menopause • RA rare in men below age 35 Both genetic and environmental factors play a role in the initiation of RA | Influence of Age and Gender |
| Inc RF of RA: • Studies compared to Caucasians o Higher prevalence in Native Americans o Lower prevalence in African Americans and Asians | Influence of Ethnicity |
| Inc RF of RA: Familial tendencies seen in 60% of cases Increased risk for Nulliparous Increased risk of onset during post-partum period • Breast feeding associated with increased Prolactin Decreased risk with oral contraceptive use | R/T Hormones and Hormonal Changes |
| Risks assoc w/ RA, through increased incident of: | • Cardiovascular morbidity: don’t know, only cardiovascular problems. o Corticosteroids • Lymphoma: Non-Hodgkin |
| Risk assoc w/ RA: using medications like (3 types) - first line trx, especially what type? - joints affected, need intra-articular injection - DMARDS stands for? | - NSAIDS: COX Inhibitors - Corticosteroids - DMARDS: Disease Modifying Anti-Rheumatic Drugs |
| The 3 main, current, & identifiable ENVIRONMENTAL Factors of RA Incidence and prevalence is what? | 1 - Diet 2 - Cigarette Smoking 3 - Occupation |
| Mortality Rate of RA: -what % of 10-yr survival after what? -All causes of death are increased except for? WHY? -Mean life expectancy & quality adjusted? | -80% after diagnosis - GI Malignancies, from prophylactic proton pump inhibitors -Mean - 18.6 years and quality adjusted is 11.3 years |
| List the 7 types of drugs increasing risk associated with RA: | 1: NSAIDS 2: ASA 3: Methotrexate 4: Plaquenil (Hydroxychloroquine) 5: Gold Salts 6: Anakinra: BMR's = Biologic Response Modifiers 7: Tetracyclines - Antibiotics |
| What drug is useful in the first few weeks after the onset of symptoms while a diagnostic workup is undertaken. Useful as bridge therapy while waiting for slow-acting DMARDs to become effective | NSAIDS |
| What drug Responds to high dosages <2 gm/day relieves pain only 4-6 gm/day required to get relief from RA inflammation – not realistic! Not going to give, therefore it doesn’t work, may help relieve pain while waiting for other meds to work. | ASA |
| What drug is antimalarial, preferred DMARD for pt w what? -has a delayed onset and therapeutic effect take months develop. | Plaquenil Preferred for pt's with mild s/s |
| What drug's Mech of action not well established, may include the reduction of circulating B cells.Risk of toxicity – they are injectable – give to pt. not responding to DMARD’s or NSAIDS • Mucocutaneous reactions • Proteinuria • Cytopenias | Gold Salts |
| Biologic Response Modifiers (BRM) Ex: Embrel & is Newest class for treatment of RA. Inhibitor of pro-inflammatory cytokine:inhibiting chemical messengers. Effective as monotherapy and in combination with Methotrexate. SE: Skin sensitivity/infections | BRM: Anakinra |
| Drug's that Also have anti-inflammatory and immunomodulatory properties o Minocycline – 200mg/day | Tetracyclines: Antibiotics |
| What is the Chronic, autoimmune, connective tissue disorder involving the skin and other organs - Exacerbations and remissions - Unknown etiology, may be genetic, immune or environmental factors | Scleroderma: Systemic Sclerosis |
| Patho of Scleroderma: Overproduction of ___ leads to __ & __ resulting in damage to affected areas. What is responsible for scar tissue formation? Deficiency makes skin __ & non-___, will become extremely___from ___ collagen formation | Collagen Fibrosis & Inflammation Collagen Elastic, non-flexible, tight from INCREASED |
| 2 main types of Scleroderma are | Systemic Sclerosis CREST Syndrome |
| Type that involves skin of fingers, hands, face and trunk and visceral organs. May be life-threatening d/t affecting lung expansion – don’t want collagen in lung cavity | Systemic Sclerosis |
| Abn dep Ca salts skin? Exag resp of hands & ft-cold, digits painful, turn white, blue, & red: vasoconstr from dec perf: AKA? collagen deposits in esophagus=diff swallowing? scl. local fingers? sm, dil bl ves w/ bright-red cntr pt, spiderlike branc | CREST Syndrome: Calcinosis Raynauds Syndrome: Patriotic Disease Esophageal Dysfunctions Sclerodactyly Telangiectasia |
| S/S of Scleroderma on: -Skin, Lips, Hands/Feet, - Joints - Intestinal - Heart - Lungs - Kidneys | Skin: Shiny, thick on fingers, arms trunk and face, Non-Pitting Edema affected areas, Ca dep,Telangiectasia, Hyperpigmentation - Pursed lips brx Joint stiff, GI: const, dia, malabsorption syn, Heart: Pericarditis, Lungs: SOB on exertion, Kid: RF |
| 4 methods of trx for Scleroderma: | NSAIDS H2antagonists and proton pump inhibitors Beta blockers and calcium channel blockers – it can affect the heart in the visceral area Corticosteroids and immunosuppressive drugs |
| - Lack of one or more components of the immune system results in immunodeficiency disorders | Immunodeficiency Diseases |
| What was first recognized in 1981 & Caused by a virus (the human immunodeficiency virus) that destroys helper T cells and that is harbored in macrophages and monocytes. o What helps in immune response, if destroyed, decreased immune system. | AIDS: Helper T Cells |
| AIDS virus can also damage tissues of the what and what and produce progressive what? | Damage tissues of spinal cord and brain produce progressive dementia |
| What is Secondary immunodeficiency disorder? Main effect of HIV causing destruction of? | AIDS Destruction of CD4 + T Cells |
| 3 Phases of AIDS? 3 Types of AIDS? | 3 Phases of AIDS: 1. Primary HIV 2. Latency 3. Overt AIDS Types: 1 - HIV Type 1 2 - HIV Type 2 3 - Transmission of both in the same |
| What type is responsible for most of the HIV infections worldwide? | HIV Type-I |
| What type is endemic in many countries in West Africa; rare in other parts of the world; spreads more slowly and causes disease more slowly than HIV – I | HIV Type-II |
| HIV:_____ ____= ___ ___ was discovered in 1983 RNA viruses are called ______ because they replicate in a “_____” manner. (Going from what to what) Also Known As? | Ribonucleic Acid: RNA Retroviruses Backwards Going from RNA to DNA Reverse Transcriptase: when it's going backwards |
| HIV must be where to replicate? Enters the cells how? | Like all viruses, HIV must be inside the cell to replicate HIV enters the cell when the proteins gp120 “knobs” on the virus bind to CD4 receptor sites on the cell |
| Once inside the cell, viral RNA is transcribed to viral __ and enters the cell’s ____ Upon entering the nucleus it becomes a permanent part of the what? | DNA Nucleus Cell's Genetic Structure |
| 2 consequences of viral RNA to DNA is? | 1). All daughter cells from this cell will be infected (b/c all genetic material is replicated in cellular division 2). The cell’s genetic codes direct the cell to make new viral RNA (HIV) with the assistance of the enzyme Protease |
| HIV infects cells that have __ _____ on their surfaces; These include what 2 types of cells? | CD4 Receptors • Lymphocytes • Monocytes/macrophages |
| CD4 Counts (normal range is? What takes advantage of the low CD4 count to infect the body & begins when CD4 falls below 200 cells/mm3? With major concern r/t? | N = 1,000 - 2,000 CD4/mm3 Opportunistic diseases R/T immune suppression – most of the time, its not the HIV virus that kills the pt, it’s the infections they get from having the virus. |
| ONSET of HIV: ____weeks later = get Syndrome known as? Begin having S/S of: • Then, ___ yrs. • Latency, then ____ years onset of AIDS: | 2-4 weeks later = Acute Clinical Syndrome Begin having S/S of general malaise, fever, chills; think it’s a cold. • Then, 8-10 yrs. • Latency, then 2-3 years onset of AIDS: |
| What is the development of evidence of an antibody response to a disease or vaccine? | Seroconversion |
| What is the Time after infection and before Seroconversion? - During this period, all HIV-infected persons can transmit the virus through the blood; unprotected sex; offspring during L&D; pregnancy; and lack of using universal precautions | Window Period |
| What is the Development of HIV-specific antibodies occurs Seroconversion Accompanied by flulike symptoms. Known as Acute Retroviral Syndrome Generally occurs 1-3 weeks after initial infection and lasts for 1-2 weeks | Acute Infection |
| • Median time frame 10 years • CD4+ T lymphocytes >500 and the viral load is Low – amt of HIV virus in blood • May be asymptomatic or have vague symptoms | Early Chronic Infection |
| • CD4+ T cell count drops to 200-500 • Viral load begins to rise AIDS diagnosis when one of the following occurs: HIV is when infected with virus, AIDS is full-blown syndrome? | Late Chronic Infection |
| • CD4+ T cell count below 200 • Development of opportunistic infections • Development of opportunistic cancers • Wasting syndrome – no muscle tone, sunken eye/skin • *Associated dementia | Late Chronic Infection |
| Pneumocystis Carinii Pneumonia (PCP) – does not cause pneumonia in healthy people only people with HIV/AIDS TB – increase in TB in HIV/AIDS pt. from suppressed immune system. • 2 most common respiratory illnesses associated with AIDS? | Respiratory Infections |
| Diagnosis of HIV Infection • Tests that detect HIV specific antibodies & Major problem is? Do thorough health history, lifestyle, most important to educate | Major Problem - Window Period Dx Testing |
| screening test, generally do two tests if +, first test run on pt.’s, progress to? | ELISA or EIA |
| confirmatory test o HIV is diagnosed when both + from both tests | Western Blot |
| Oral specimen collection devise (same as ELISA) - draws out ____ from gums; not a __ test, checks for antibodies; virus not located in saliva? Finger stick with results in 20 minutes; confidential? Retest at __months d/t"__" & if thinking they are expos | Orasure, draws out antibodies, not a saliva test, Home Access Test: OraQuick 3-6 Months d/t "Window Period" |
| The progression of HIV is monitored by what? Inc/Dec? Lab tests that measure viral activity allow better what? | CD$ + T Cell Counts: Both decrease with the disease Allow better assessment of the patient’s status and disease progression |
| What counts the # of viral particles in a blood sample & helps to determine when to initiate therapy? | Viral Load Counts |
| 3 Main goals of HIV therapy: - Decrease what? - Maintain/Increase what? - Delay what? | •Decrease HIV RNA viral loads •Maintain or Increase CD4+ T levels to > 200 •Range of 800-1200 preferred for HIV pt.’s •Delay the development of symptoms |
| In general drugs used to treat HIV are what type of drugs? They work at different point in the replication cycle •No drug to date can ___ HIV, but therapy can ___ viral replication and ____ progression | Anti-Retroviral Drugs Cure Decrease Delay |
| 5 Main groups of meds that treat HIV are? | 1- Reverse Transcriptase Inhibitors 2- Protease Inhibitors 3- Fusion Inhibitors 4- Nucleosides/NRT's: Nucleotide Reverse TRanscriptase Inhibitors 5- Non-Nucleoside Reverse Transcriptase Inhibitors |
| Which group of meds contains 1. Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTI’s) 2. Non-Nucleoside Reverse Transcriptase Inhibitors and These 2 affect the Early Stages of replication? | Reverse Transcriptase Inhibitors |
| Which group of medicines affects Late Stages of replication, Interferes with the activity of the protease enzyme. Most Effective antiretroviral drugs available, Resistance can be a big problem; contraindicate St Johns Wort & Depression? | Protease Inhibitors |
| Which group of meds Inhibits binding, prevents entry of HIV into cells, Enfuviritide (Fuzeon) – currently only fusion inhibitor available, and Blocks entry of HIV into CD4 T cells? | Fusion Inhibitors |
| First line trx of drugs that inhibit in the beginning, First drugs used against HIV and constitute the backbone of treatment, To be effective they must undergo conversion to their active form, Cause premature termination of the growing DNA strand? | Nucleoside/Nucleotide Reverse Transcriptase Inhibitors: NRTI's |
| Which group of meds are active as administered Bind to reverse transcriptase and cause direct inhibition? | Non-Nucleoside Reverse Transcriptase Inhibitors |
| Because different drugs act on different stages of the replication cycle, optimal treatment includes a combination of at least three drugs, often referred to as? | HAART:Highly Active Anti-Retroviral Therap |
| The main goal of HAART is? | Sustained suppression of HIV replication, undetectable viral load, & increasing CD4+ cell count |
| How do we know the meds are working in CBC count, Viral Load, CBC & what are we checking for? | CD4 cell count:In HIV(+)person-CD4 is 800-1200 cells per mm3. Viral load:measures more than 10-30,000ml/bl; goal-make low as poss. CBC:A dec drop RBC & WBC, HIV infection getting worse/meds. |
| Main Function for: Bind to the cells infected with the human immunodeficiency virus (HIV) Used in clients seroconverted to HIV or exposed to occupational HIV or leukemia? | Immunomodulating Agents |
| Common SE of Immunomodulating Agents are? | Neurological: insomnia, confusion, seizures; Bone marrow depression: leukopenia, thrombocytopenia, anemia |
Created by:
ehward
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