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Pharm III Test III
Surface
| Question | Answer |
|---|---|
| What is a chronic inflammatory disease principally involving synovial membranes of joints but with extra-articular manifestations? | Rheumatoid Arthritis |
| What does the unknown etiologic agent do in RA? | initiate a nonspecific immune response |
| What is the earliest inflammatory changes in joints in RA? | inflammation and occlusion of small subsynovial vessels suggesting agent carried in circulation |
| RA begins as a inflammatory lesion and progresses to a proliferative on and destroys what? | adjacent cartilage and bone |
| What are the goals of therapy in RA? | 1) relief of symptoms, 2) maintenance of joint function and ROM, and 3) prevention of deformity |
| What is the nonpharmacologic therapy for RA? | education, psychosocial, systemic/articular rest, exercise, heat/cold, assistive devices, lifestyle/diet, and physical medicine |
| What is the Salicylate NSAID most patients are initially treated with? | Aspirin |
| Why is Aspirin usually effective? | due to anti-inflammatory action |
| What drugs are equivalent to ASA, and some respond to one better than others? | Nonsalicylate NSAIDs (COX-2 specific inhibitors, Celebrex) |
| What is Glucocorticoids mechanism of action? | Inhibit synthesis of chemical mediators; suppress infiltration of phagocytes averting damage from lysosomal enzymes; & suppress proliferation of lymphocytes reducing the immune component of inflammation |
| The anti-inflammatory effects of glucocorticoids are what in comparison to NSAIDs? | greater |
| What treatment is glucocorticoids indicated for? | adjunctive treatment of acute exacerbations of RA with generalized symptoms |
| When may Glycocorticoid injections be used? | When one or two joints are effected |
| What type of use should oral administration of Glucocorticoids be restricted to? | Short-term therapy whenever possible, most often given to provide relief until drugs with slower onset can provide control |
| Who should Long-term therapy of glucocorticoids be given to? | limited to those who have failed to respond adequately to all other forms of treatment |
| What are the adverse effects of Glucocorticoids? | adrenal insufficiency, osteoporosis, infection, glucose intolerance, myopathy, fluid and electrolyte disturbances, growth retardation, psychologic disturbances, cataracts, peptic ulcer disease, iatrogenic Cushing's Syndrome |
| who is Glucocorticoids contraindicated in? | those with systemic fungal infections and those receiving live-virus vaccines |
| How is Glucocorticoids D/C? | slowly; tappered off |
| What DMARD agent is considered first-line agent for most patients with RA? | Methotrexate |
| How quick is Methotrexate's onset of action? | Relatively rapid; therapeutic doses (6-8 weeks) |
| The majority of patient's continue to take Methotrexate for how many years and why? | 5 years; and because of its efficacy and tolerability |
| What is Methotrexate effective in treating? | reducing signs and symptoms of RA and slowing or halting radiographic damage, psoriatic arthritis and other spondyloarthopathies, and many other autoimmune diseases |
| What is Methotrexate's mechanism of action? | Anti-inflammatory effects are related to interruption of adenosine and possible effects on TNF pathways. Immunosuppressive and toxic effects are due to inhibition of an enzyme involved in the metabolism of folic acid, dihydrofolate reductase |
| What is the dosage for Methotrexate? | Starting at 10mg per week; increased to 20mg by week 8; Max dose is 25mg per week |
| How is Methotrexate administered? | PO or SQ |
| What much you check prior starting a patient on Methotrexate? | Renal insufficiency, acute or chronic liver disease, significant ETOH intake or abuse, leukopenia, thrombocytopenia, or untreated folate deficiency |
| What effect does Salicylates and other NSAIDs and Trimethoprim (Bactrim & Septra) have on Methotrexate? | They block the renal excretion of Methotrexate |
| Can Methotrexate be administered with NSAIDs? | Yes, as long as liver function tests are closely monitored |
| What are the usual time for Methotrexate to take effect? | As early as 4-6 weeks |
| What trial is suggested in patients starting Methotrexate? | a trial of 3-6 months at an increased dose (e.g. 20mg/wk) |
| What side effects are seen with Methotrexate? | Hepatic cirrhosis, interstitial pneumonitis, severe myelosuppression, stomatitis, oral ulcers, mild alopecia and hair thinning, GI upset, HA, fatigue, feeling "wiped out" (Methotrexate fog) |
| What tests should be done prior to starting Methotrexate? | CBC, liver chemistries, serum creatinine, hepatitis B and C serologies, and CXR |
| What routine tests should be done while taking Methotrexate? | CBC, liver profile, serum albumin, and serum creatinine every 4-8 weeks |
| What should patients limit their ETOH intake to while taking Methotrexate? | no more than 2 per week |
| What can be a risk while taking Methotrexate? | increased risk of herpes zoster infection (shingles), cancer risk, lymphoma |
| Due to Methotrexate being tetrogenic, how does this effect contraception? | Women should discontinue the drug one ovulatory cycle prior to attempting conception and males should wait 3 months. |
| What is antimalarial drug used to treat RA, that is relatively safe and well tolerated? | Hydroxychloroquine (Plaquenil) |
| What patients should this Plaquenil be given to? | limited to those with very mild and nonerosive disease; has a limited ability to prevent joint damage on its own |
| What other drugs can Plaquenil be combined with? | Methotrexate and Sulfasalazine |
| What is Plaquenil's mechanism of action? | unknown; thought to involve changes in antigen presentation or effects on the innate immune system |
| Why is Plaquenil not commonly used? | greater toxicity on the eye |
| What is the dosage of Plaquenil? | 400mg/day but sometimes 600mg/day; once per day or divided twice per day |
| When is Plaquenil's usual time to effect? | 2-4 months; if no response after 5-6 months should be considered drug failure |
| What are the side effects of Plaquenil? | toxicities on the eye, corneal deposits, extraocular muscular weakness, loss of accommodation and sensitivity to light, a retinopathy that may progress to irreversible vision loss |
| How often are ophthalmologic exams required while taking plaquenil? | Baseline and then follow-up every 12 months |
| How effective is Sulfasalazine (Azulfidine) in comparison to Methotrexate? | somewhat less effective |
| How does Sulfasalazine treat RA? | reduce signs and symptoms and slows radiographic damage |
| What medications can Sulfasalizine be given with as part of a triple therapy to provide benefits to those who have had inadequate responses to methotrexate alone? | Methotrexate and Hydoxychloroquine |
| What other disorders is Sulfasalazine used to treat? | Inflammatory bowel disease and spondyloarthropathies |
| What may some of Sulfasalazine's effects be due to? | folate depletion |
| What is the usual dosage for Sulfasalazine? | 2-3 grams per day twice a day; may be starting at 1 gram per day and increased as tolerated |
| What is the usual time for effect for Sulfasalazine? | 6 weeks to 3 months |
| What side effects may Sulfasalazine cause? | hypersensitivity and allergic reaction to those allergic to sulfa, GI complaints, mild cytopenias |
| What lab tests may be needed prior to the start of Sulfasalazine? | Screened for a deficiency of enzyme glucose-6-phosphate dehydrogenase (G6PD) which may predispose pt to RBC hemolysis and anemia, Liver function tests-drug my increase levels, blood monitoring every 1-3 months depending on dose |
| Which drug is similiar in efficacy to Methotrexate in terms of S/S, and is a viable alternative to patients who have failed or are intolerant to Methotrexate? | Leflunomide (Arava) |
| Can Arava slow radiographic progression of RA? | True |
| Which drug can Arava be combined with to treat patient's with NO preexisting liver disease, as long as the liver function tests are carefully monitored? | Methotrexate |
| Which other disease has Arava been studied in, with some efficacy demonstrated? | Psoriatic arthritis |
| What is Arava's mechanism of action? | May be related to ability to inhibit de novo pyrimidine biosynthesis through the inhibition of the enzyme dihydroorotate dehydrogenase. Also has effects on stimulated T cells |
| Is the half-life of Arava long or short? | Very long, extensively bound and undergo further metabolism before excretion |
| What is the dosage of Arava? | 10-20 mg/day; may be reduced to 10 mg daily if not tolerated at 20 mg |
| What is the usual time for Arava to effect? | Relatively rapid; 4-8 weeks |
| What are the side effects of Arava? | mild diarrhea, GI upset, alopecia and hair thinning |
| What is the only contraindication for patients taking Arava? | Arava has teratogenic effects, extreme care must be taken for treatment of women of child bearing potential; women should be warned about the possible risk to fetus and cautioned to use adequate birth control |
| What monitoring should be done for patients taking Arava? | CBC, hepatic panel (at least every 2 months) |
| What is a pro-inflammatory cytokine, produce by macrophages and lymphocytes and is found in large quantities in the Rheumatoid joint and produced locally in the joint by synovial macrophages and lymphocytes infiltrating the joint synovium? | Tumor necrosis factor alpha (TNF) inhibitors |
| What effect does TNF have on joint damage and destruction? | it is one of the critical cytokines that MEDIATE joint damage and destruction due to its activities on many cells in the joint as well as effects on other organs and body systems |
| What effects do TNF inhibitors have on RA? | decrease signs and symptoms, slowing or halting radiographic damage, and improving function and quality of life |
| What other disorders has TNF inhibitors been approved to treat? | Psoriatic arthritis and Ankylosing spondylitis |
| What are the names of the three TNF inhibitors approved for treatment of RA? | Etanercept (Enbrel), Infliximab (Remicade), Adalimumab (Humira) |
| Which drug is a fusion protein that combines two extracellular binding domains of the p75 form of the TNF receptor with the Fc portion of a human IgG1 antibody molecule? | Etanercept (Enbrel) |
| When used as a monotherapy or in combination with Methotrexate, Enbrel has what effect on treating RA? | reduces the signs and symptoms, and slows or halts the radiographic damage |
| What other disorders is Enbrel approved to treat? | Psoriatic arthritis, Ankylosing spondylitis, and psoriasis |
| What is Enbrel's mechanism of action? | it binds to TNF in the circulation and in the joint, preventing interaction with cell surface TNF receptors thereby reducing TNF activity |
| What is the dosage of Enbrel? | 50 mg/week or 25 mg/ twice per week |
| How is Enbrel administered? | SQ |
| What is the half-life of a 25 mg dose of Enbrel? | 70 hours |
| What is Enbrel's usual time to effect? | 1-4 weeks to 3-6 months |
| What are the side effects seen with Enbrel? | increased risk of infection, upper respiratory symptoms, positive ANA, serious and opportunistic infections, lymphomas, non-Hodgkins lymphomas, transient neutropenia, other blood dyscrasias, injection site reactions |
| What screening is recommended prior to starting a patient on any TNF inhibitor? | screening for latent TB |
| What patient's is TNF inhibitors not recommended in? | demyelinating disease and congestive heart failure |
| What is a chimeric monoclonal antibody that binds TNF with high affinity and specificity? | Infliximab (Remicade) |
| in combination with Methotrexate, what is Remicade used to treat? | RA, psoriatic arthritis, ankylosing spondylitis, psoriasis, Crohn's disease |
| The antibody binding site for TNF of Remicade is where? | of mouse origin. with the remaining 75% of the remicade antibody derived from a human IgG1 antibody sequence |
| Although Remicade is effective as a monotherapy in reducing S/S, what may develop and reduce the durability of the response? | anti-infliximab antibodies |
| Co-treatment with what may reduce the frequency of anti-infliximab antibodies and is recommended with infliximab? | Methotrexate |
| What is the combination of Methotrexate and Remicade effective in treating? | reducing clinical manifestations and slowing or halting the radiographic progression of the disease |
| What is Remicade's mechanism of action? | it binds TNF in the joint and circulation, preventing its interaction with TNF receptors on the surface of inflammatory cells, and eventually clearing TNF from the circulation. Monoclonal antibodies also bind to TNF. Remicade inhibits the activity of TNF |
| In what way is Remicade administered? | IV and typically take 2-3 hours |
| What is the dosing of Remicade? | Starting dose-3mg/kg; additional dosing at 2-6 weeks, then every 8 weeks after that; Maximum dose-10 mg/kg; frequency of infusion increased every 4-6 weeks |
| What is Remicade's usual time to effect? | days to weeks |
| What are the side effects of Remicade? | increased infections, sepsis, disseminated TB, opportunistic infections, fever, chills, body aches, HA, ANA, anti-double stranded DNA antibodies, SLE-like syndromes |
| The risk for Disseminated TB is what in Remicade in comparison to Etanercept? | increased due to longer half-life |
| How may the infusion symptoms of Remicade be reduced? | preadminister diphenhydramine (Benadryl), acetaminophen, and sometimes corticosteroids, or slowing the infusion |
| What drug is a fully human anti-TNF monoclonal antibody with high specificity for TNF? | Adalimumab (Humira) |
| Like other TNF inhibitors, is effective as monotherapy or in combination with Methotrexate, how does Humira treat RA? | reduces S/S, and slowing or halting the progression of the disease |
| How, and when is Humira administered? | SQ injections, every two weeks, can be increased to weekly if needed. |
| What other disorders is Humira approved to treat? | RA, Psoriatic arthritis, ankylosing spondylitis, and Crohn's disease |
| What is Humira's mechanism of action? | binds specifically to TNF and blocks its interaction with the p55 and p75 cell surface TNF receptors, thereby interfering with endogenous TNF activity. Adalimumab binds to both soluble as well as cell bound TNF |
| What is the current dosage of Humira and how is it administered? | 40 mg SQ every other week; may be increased to weekly if needed |
| What is the half-life of Humira? | approximately 2 weeks (10-20 days) after 40 mg dose |
| How long is Humira's usual time to effect? | 1-4 Weeks |
| What are the side effects of Humira? | increased infections; upper respiratory tract infections; bronchitis; UTI; TB as reactivation of latent disease; positive ANA titers; lupus-like disease; lymphomas; injection site reactions |
| What drug is the first of a class of agents known as T-cell costimulatory blockers that interfere with the interactions between antigen-presenting cells and T lymphocytes and affect early stages in the pathogenic cascade of events in RA? | Abatacept (Orencia) |
| If the T cells in Orencia recognize antigens as foreign and they receive a second stimulus, they will become active and what? | proliferative, traffic to inflamed sites, and secrete proinflammatory cytokines including TNF. |
| With Orencia, one of the important second signals for T cells activation is mediated by what? | molecules CD80 and CD86 found on antigen presenting cells and the CD28 molecule on the T cell surface |
| What is Orencia's mechanism of action? | a fusion protein that combines the extracellular domain of the molecule CTLA4(CD154) with the Fc portion of a human immunoglobulin molecule. When binds to CD28 on Tcell surface, it prevents the second signal from being delivered, decreasing Tcell response |
| What are additional effects of Orencia's mechanism of action? | decreasing the production of T cell derived cytokines including TNF |
| What is Orencia's dosing? How often? And how is it administered? | IV; once per month; based on body weight; <60 kg receiving 500 mg, 60-100 kg receiving 750 mg, and >100 kg receiving 1000 mg |
| When does Orencia typically take effect? | within 3 months; continue to show improvements through the first year |
| what are the adverse effects of Orencia? | increased infections; respiratory infection; pneumonia; malignancies; opportunistic infections; mild infusion reactions |
| What are important inflammatory cells with multiple functions in the immune response, that serve as antigen presenting cells & can secrete cytokines, and differentiate into antibody-forming plasma cells? | B cells |
| Why is B-Cell depletion (Rituximab [Rituxan]) effective in RA? | reduces S/S and slows radiographic progression |
| Aside from RA, what other disorders has Rituxan been approved to treat? | Non-Hodgkin's Lymphoma & malignant conditions of the lymphocytes and lymph nodes |
| What patient's are approved to take Rituxan? | Those who have failed DMARD therapies and those who have failed TNF antagonists |
| What is Rituxan's mechanism of action? | Chimeric monoclonal antibody that binds to the CD20 molecule on B cell surface that leads to B cell removal from circulation. Levels of autoantibody rheumatoid factor decrease but other antibodies levels remain in normal range |
| What is Rituxan's time of onset? | up to 3 months; effects may last 6 months to 2 years following single infusion |
| What is the dosing of Rituxan and how is it administered? | 1000 mg IV over 3-4 hours with two doses given 2 weeks apart. Give corticosteroids with each infusion and premedicate with Diphenhydramine and Acetaminophen |
| What are the adverse effects of Rituxan? | Infusion reaction-hives, itching, swelling, difficulty breathing, fever, chills, changes in BP; Increased infections; reactivation of viral infections that were dormant (Hep B); progressive multifocal leukoencephalopathy; potentially fatal brain infection |
| What should patients prior to starting Rituxan and what should be avoided? | Immunizations should be completed and live viruses should be avoided |
| What drug is a human recombinant IL-1 receptor antagonist and is approved for the treatment for RA? | Anakinra (Kineret) |
| Anakinra can be used as a monotherapy or in combination with what drugs? | DMARDS other than TNF blocking agents |
| Why is Anakinra not recommended for combination with TNF inhibitors? | studies have shown infections without additive clinical benefit |
| What is Anakinra's mechanism of action? | it blocks the biologic activity of IL-1 by binding to IL-1R type I with the same affinity as IL-1 beta |
| What is the typical dosage for Anakinra and how is it administered? | 100 mg/day and SQ |
| How long is Anakinra's time to effect? | 2-4 weeks |
| What are the side effects of Anakinra? | injection site reactions-erythema, itching, discomfort; risk of serious infection; decreases in absolute neutrophil counts |
| What drug is effective in the treatment of RA when given IM and until the 1990s was the most often used DMARD agents but have been replaced by Methotrexate and other DMARDs as the preferred agents to treat RA? | Gold |
| What are the 2 injectable gold compounds available? | Myochrysine and Solganal |
| Why are gold compounds now rarely used? | numerous side effects, monitoring requirments, limited efficacy, very slow onset of action |
| What oral gold compound is now available? | Auranofin |
| What is the dosage of Gold | 10 mg IM, 25 mg second week, 50 mg weekly until a response has occurred or until a total of 1 g has been given; If favorable response, therapy is tappered to 50 mg Q 2 weeks for 3 months, then Q 3 weeks for 3 months, then finally monthly maintenance dose |
| What is Gold's usual time to effect? | 4-6 months or after administration of 1 g of gold |
| What are the side effects of Gold? | rash*; severe exfoliative dermatitis; ulcerations and mucositis of mouth, tongue, and pharynx, mild proteinuria, glomerulonephropathy, isolated microscopic hematuria, immune thrombocytopenia, granulocytopenia, aplastic anemia, nitritoid reaction;blue skin |
| What tests should be done prior to starting Gold? | CBC, urine test for protein |
| What drug is a purine analog that can cause bone marrow suppression and lowering of blood cell counts (WBC, WBC, and platelets) particularly in patients with renal insufficiency or when used concomitantly with allopurinol or ACE inhibitors | Azathioprine (Imuran) |
| When may a patient see effects from Imuran? | May take 8-12 weeks and has some activity in RA |
| What screening is recommended before initiating therapy with Azathiprine? | screening for levels of the enzyme thiopurine methyltransferase (TPMT) |
| What blood tests are necessary for patients taking Azathioprine? | blood counts and liver function tests |
| What are side effects of Azathioprine? | nausea and alopecia |
| What drug is an immunosuppressive agent approved for use in preventing renal and liver transplant rejection and also has activity in psoriasis and other autoimmune diseases and has some activity as a disease modifying therapy in RA? | Cyclosporine (Sandimmune, Neoral) |
| What other drug may Cyclosporine be combine with? | Methotrexate |
| How does Cyclosporine inhibit T cell function? | by inhibiting transcription of interleukin-2 |
| What are the main toxicities of Cyclosporine? | infection and renal insufficiency |
| What monitoring is needed while taking Cyclosporine? | Renal function and blood pressure |
| What risks are increased while taking Cyclosporine? | increased blood pressure; infection; malignancies including lymphoma |
| What rug is a potent immunosuppressive agent that is reserved for severe cases of refractory RA and those with manifestations such as Vasculitis? | Cyclophosphamide (Cytoxan) |
| What other disorders has Cytoxan been approved to treat, aside from RA? | Vasculitis and lupus |
| What must be carefully monitored due to the serious toxicities while taking Cytoxan? | Blood counts |
| What are the serious toxicities of Cytoxan? | bone marrow suppression, hemorrhagic cystitis, premature ovarian failure, infection and secondary malignancy particularly an increased risk of bladder cancer |
| Which drug is primarily prescribed for patients with persistently aggressive RA who have failed other available DMARDs? | D-Penicillamine (Cuprimine, Depen) |
| What are the major side effects of Depen? | severe rash, effects on renal function, lupus like illness |
| What must be carefully monitored while taking Depen? | Kidney function |
| What allergy is contraindicated with Depen? | Penicillin |
| What type of sedation induces an altered state of consciousness that minimizes pain and discomfort through the use of pain relievers and sedatives? | Conscious sedation |
| What are patients under conscious sedation able to do? | speak and respond to verbal cues throughout the procedure, communicating any discomfort they experience |
| What may occur do to conscious sedation? | A brief period of amnesia that may erase any memory of the procedure |
| Where is conscious sedation administered? | hospitals, outpatient facilities, ambulatory surgery, doctors offices, etc. |
| When is conscious sedation administered? | biopsy, vasectomy, minor foot surgery, minor bone fracture repair, plastic/reconstructive surgery, endoscopy, diagnostic studies and tx of the stomach, colon, & bladder, radiation, bone marrow aspiration |
| What must be done prior to conscious sedation? | assessment of medical conditions that interfere with sedation, risk factors, past medical history, severe heart/lung disease |
| Who can administer conscious sedation? | certified registered nurse anesthetists, anesthesiologists, physicians, dentists, oral surgeons, specifically trained RNs |
| What must be monitored throughout and after the procedure do the risk of slipping into a deep sleep? | HR, BP, breathing, oxygen, alertness, oxygen saturation & pulse oximeter is the most important |
| What is the most sensitive parameter affected during increased levels of conscious sedation? | oxygen saturation |
| How often should vital signs be assessed before, during, and after conscious sedation? | once before, a minimum of every 5 minutes during the procedure, and every 15 minutes for the first hour after the procedure, and then as needed |
| What equipment must be immediately available during conscious sedation? | airway equipment, resuscitative medications, suction apparatus, supplemental oxygen delivery systems, medication reversal agents |
| What are the side effects of conscious sedation? | amnesia, HA, hangover, nausea, vomiting, unpleasant memories of the surgical experience |
| What is the criteria to D/C conscious sedation? | stable V/S and O2 sat, positive gag reflex, cough, and swallow, alert and appropriate to baseline, can sit unaided, walk with assist, minimal N/V, adequate hydration, dressing checked etc., physician order for discharge |
| What are the instructions after conscious sedation? | Do not drive a vehicle or operate dangerous equipment or make any important decisions for at least 24 hours after conscious sedation |
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