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characterization essay Care plan development. •• select medication therapy that will likely achieve goal iop with minimal adverse effects. •• use combination glaucoma eye drops when possible to improve adherence. •• address patient concerns about glaucoma and its treatment. •• educate patient on importance of medication adherence. Instruct patient on how to instill eye drops and have them demonstrate their technique. Follow-up evaluation. •• follow-up in 2 to 4 weeks to reassess patient for progression in glaucomatous damage, achievement of target iop, adherence, and presence of adverse effects to medication therapy. Review interval medical history. Perform/review ophthalmic examination findings. Chapter 61  |  glaucoma  933 primary angle-closure glaucoma follow-up of acute angle-closure crisis occurs in the postoperative period.

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why do i deserve this scholarship essay sample Thromb ha~most 1997;78(suppl):724. Saxonhouse ma. Burchfield dj. The evaluation and management of postnatal thromboses. ] p~rinat 2009;29(7):467--478. Schmidt b, andrew m. Neonatal thrombosis. Report of a prospective canadian and international registry. P~diatrics 1995(5);96:939-943. Werlin sl, lausten t, jessen s, et al. Treatment of central venous catheter occlusions with ethanol and hydrochloric acid.] parent ent nutr 1995;19:416-418. Yangjy, chan ak, callen dj, et al. Neonatal cerebral sinovenous thrombosis. Sifting the evidence for a diagnostic plan and treatment strategy. P~diatrics 2010;126(3). E693-e700. Young te, mangum b. N~ofax 2008. Montvale, nj. Thompson-reuters. 2008. Anemia helen a. Christou i. Hematologic physiology of the newborn { 1-5). Significant changes occur in the red blood cell (rbc) mass of an infant during the neonatal period and ensuing months. The evaluation of anemia must take into account this developmental process, as well as the infant's physiologic needs. A. Normal development. The physiologic anemia of infancy (1) 1. In utero, the fetal aortic oxygen saturation is 45%, the erythropoietin levels are high, and the rbc production is rapid.

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thesis binding perth Diagnostically, aqp4-antibody testing is an extremely sensitive and speci c modality by which to pinpoint nmo. A de nitive diagnosis o nmo also requires that at least 2 o the ollowing criteria be met. Nmo-igg seropositivity, brain mri inconsistent with ms, and spine mri showing a contiguous spinal lesion encompassing at least 3 vertebral segments. T ere are no curative treatment modalities or nmo. Instead, treatment ocuses on reducing symptom relapse and severity through longitudinal immunosuppression as prophylaxis. Methylprednisolone, intravenous immunoglobulin (ivig), or cyclophosphamide therapies are o en used to treat relapses. For chronic immunosuppression, corticosteroids, azathioprine, and rituximab are commonly employed. Additionally, monoclonal antibody treatment is currently under investigation as a potential new avenue o medical therapy. Without curative therapy, nmo is a progressive and severely debilitating disease. T ere ore, it is imperative that a diagnosis is made quickly and immunosuppressive therapy is started as soon as possible.7 paraparesis/quadriparesis transverse myelitis xt ransverse myelitis is characterized by in ammation in the spinal cord that can cause moderate-to-severe weakness (paraparesis or quadriparesis depending on the level 443 o spinal cord involved) and disability. T e symptoms o transverse myelitis develop over a period o hours to days and are typically exacerbated over the course o subsequent weeks. Most cases develop acutely, although subacute cases have been documented. A typical presentation consists o weakness, sensory de cit, and autonomic dys unction, depending on the exact location o the spinal lesion. Weakness most o en targets leg exors and arm extensors in a pyramidal distribution. Although weakness most o en presents bilaterally due to the transverse nature o the injury, it is important to note that this is not always the case. T e term “transverse” re ers to an area o abnormal sensation at the dermatome corresponding to the cord lesion. History and physical examination are the most important diagnostic tools regarding transverse myelitis. For instance, in brown-séquard syndrome, a patient presents with characteristic motor weakness due to a unilateral lesion o the spinal cord resulting in dorsal column dys unction on the ipsilateral side and spinothalamic dys unction on the contralateral side o the lesion. Conversely, a central lesion can present with spinothalamic de cits, autonomic dys unction, and pyramidal weakness in erior to the lesion level. Meanwhile, in an anterior spinal cord syndrome, acute accid weakness may be observed with preserved dorsal column unction and spinothalamic dys unction. Once myelopathy is suspected, mri is the chosen imaging modality (figure 28-4), with c myelogram serving as an acceptable alternative. A lumbar puncture (lp) is o en per ormed to determine whether in ammatory markers are present within the csf. I imaging and csf ndings indicate cns in ammation, then the di erential must include demyelination, in ection, and autoimmune etiologies. More avorable outcomes tend to arise rom cases that are most rapidly diagnosed and treated. I csf analysis shows a bacterial or viral etiology, then the patient should be promptly started on an appropriate antimicrobial regimen. For bacterial meningitis, dexamethasone can be used prior to or along with the rst course o antibiotics. I an autoimmune, neoplastic, or in ammatory process is suspected as the cause or cord compression, intravenous methylprednisolone may be started. In re ractory cases, plasma exchange (plex) can be considered. I the appropriate treatment course is ollowed, then the prognosis o transverse myelitis is air. Factors indicating poorer prognoses include rapidly progressing symptoms such as spinal shock and back pain. Factors portending more optimistic outcomes include rapid initiation o treatment or the underlying cause o the myelitis. Chronic causes tend to have worse long-term outcomes than its acute counterparts.8 ruptured intervertebral disk xt a ruptured (herniated, prolapsed, slipped) disk (nucleus pulposus) occurs when part or the entirety o an 444 c h apt er 28 ▲ figure 28-4 axial mri cervical spine (t2 sequence) with evidence o transverse myelitis (arrow) in a 2-year-old boy who presented with quickly progressive bilateral upper extremity paraparesis with a recent viral illness. He was diagnosed with acute demyelinating encephalomyelitis (adem). Intervertebral disk erupts through a weak portion o the disk.

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essay topics for toefl Pharmacologic therapy traditional chemotherapy has been the mainstay for most lung cancer patients and will be administered to the large majority of patients, despite recent advances with targeted therapy for patients with egfr and alk mutations. Cisplatin and carboplatin are arguably the most effective traditional chemotherapy agents regardless of histology. Doublet chemotherapy regimens offer superior response rates compared with single-agent chemotherapy regimens and should be used when the patient can tolerate the increased toxicity. The effective chemotherapy agents that are added to the platinum include etoposide, paclitaxel, docetaxel, gemcitabine, vinorelbine, and pemetrexed (see table 90–4 for regimen details). Monoclonal antibodies targeting vascular endothelial growth factor (vegf) signaling (bevacizumab and ramucirumab), and epidermal growth factor receptor (egfr. Cetuximab and necitumumab) have been combined with traditional chemotherapy to improve outcomes. Tyrosine kinase inhibitors (tki) targeting egfr such as afatinib and erlotinib can be appropriate as monotherapy (usually in those patients with an egfr-activating mutation in exons 19 or 21). Similarly, tyrosine kinase inhibitors targeting an anaplastic leukemia kinase (alk) gene rearrangement (gene fusions and translocations) can be treated with crizotinib or ceritinib as monotherapy. Selecting the best regimen for a specific patient is aided by patient characteristics (ps, comorbid conditions, etc), extent of tumor spread, histology, and genetics as discussed in more detail below. Preventing and managing therapy induced toxicity (see chapter 88) is crucial to optimizing patient outcomes (eg, curing, prolonging life, or palliating symptoms). Furthermore, decisions to start chemotherapy must include the full consent and understanding of risks by the patient. Counseling on the therapeutic regimen and risk of toxicity is imperative before dosing. Lung cancer regimens and their associated toxicities are shown in table 90–4. Refer to chapter 88 for dosing recommendations in renal and hepatic failure. Treatment of small cell lung cancer sclc typically presents as extensive disease (approximately 60%–70% of new cases) and progresses very quickly. Sclcs are very responsive to chemotherapy and radiation but have a short duration of response. Radiotherapy became the standard in 1969, when a randomized trial showed that it offered the potential for patient encounter, part 3 the patient’s condition has interfered with her ability to work, but she is able to complete daily activities and has been working to this point, managing her restaurant. What is this patients ecog ps score?. Are there any nonpharmacologic interventions you would suggest?. Chapter 90  |  lung cancer  1339 table 90–4  chemotherapy regimens in lung cancer and associated toxicities13,17,19,24,33–37 neutropenia cycle length (days)   21 grade iii (%)     grade iv (%)   24 21 18 57 21 28 21 24 48 39 21 14 38 21 21 14 20 38 43 21 21 10 11 5 11 21 21     19 5–6 21 28   28 21–28 34     85 15 3 5   18 72 21 28 21 10–20 40 18 5–15 25 70 ec ic topotecan dose   carboplatin, dose targeted to auc of 6 iv (day 1), paclitaxe l200 mg/m2 iv over 3 hours (day 1), bevacizumab 15 mg/kg iv (day 1) paclitaxel 135 mg/m2 iv over 24 hours (day 1) and cisplatin 75 mg/m2 iv (day 2) cisplatin 75 mg/m2 iv (day 1) and docetaxel 75 mg/m2 iv (day 1) cisplatin 100 mg/m2 iv (day 1) and gemcitabine 1000 mg/m2 iv (days 1, 8, and 15) cisplatin 80 mg/m2 (day 1) and vinorelbine 25 mg/m2 (days 1 and 8) with or without cetuximab 400 mg/m2 initial dose. Then 250 mg/m2 weekly) cisplatin 80 mg/m2 (day 1) and vinorelbine 25 mg/m2 weekly (days 1 and 8) carboplatin, dose targeted to auc of 6 iv (day 1), and paclitaxel 225 mg/m2 iv over 3 hours (day 1) paclitaxel 200 mg/m2 iv (day 1) and gemcitabine 1000 mg/m2 (days 1 and 8) gemcitabine 1100 mg/m2 iv (days 1 and 8) and docetaxel 100 mg/m2 iv (day 8) gemcitabine 1125 mg/m2 (days 1 and 8) pemetrexed 500 mg/m2 (day 1), vitamin b12 1 mg im 1–2 weeks before treatment initiation and every 9 weeks thereafter. Folic acid 1 mg/day beginning 3 weeks before treatment initiation paclitaxel 200 mg/m2 iv over 3 hours (day 1) docetaxel 35 mg/m2 iv over 1 hour (days 1, 8, 15)   etoposide 100 mg/m2 iv (days 1–3) and cisplatin 100 mg/m2 iv (day 2) cyclophosphamide 800 mg/m2 iv (day 1), doxorubicin 50 mg/m2 (day 1), and vincristine 1. 4 mg/m2 (maximum, 2 mg) iv (day 1) etoposide 100 mg/m2 iv (days 1–3) and carboplatin auc 5–6 iv (day 1) irinotecan 60 mg/m2 (days 1, 8, 15) and cisplatin 60 mg/m2 (day 1) topotecan 1. 5 mg/m2 iv over 30 minutes (days 1–5)   other significant toxicities nausea/vomiting potential non–small cell paclitaxel–carboplatin– bevacizumab   diarrhea, fever, headache, hypertension, hemoptysis, infection, leukopenia, nausea, neuropathy, peripheral neuritis, vomiting, thrombocytopenia, thrombotic events, bleeding, proteinuria febrile neutropenia or infection, thrombocytopenia, nausea, vomiting, diarrhea, cardiac toxicity, renal toxicity, neuropathy, weakness, hypersensitivity reactions, anemia infection, thrombocytopenia, nausea, vomiting, diarrhea, cardiac, renal, neuropathy, weakness, hypersensitivity, anemia febrile neutropenia or infection, thrombocytopenia, nausea, vomiting, diarrhea, cardiac, renal, neuropathy, weakness, anemia infection, thrombocytopenia, rash, constipation, neuropathy, hepatotoxicity   high (day 1 only) neutropenia, infection, anorexia, thrombocytopenia, nausea, vomiting, dyspnea, constipation, neuropathy, anemia infection, thrombocytopenia, nausea, vomiting, diarrhea, cardiac, renal, neuropathy, weakness, hypersensitivity, anemia alopecia, nausea and vomiting, neurotoxicity, thrombocytopenia nausea and vomiting, diarrhea, thrombocytopenia, asthenia, neurotoxicity thrombocytopenia anemia infection, nausea, vomiting, diarrhea, mucositis, arthralgia, asthenia, peripheral neuropathy, alopecia, cardiovascular fatigue, nausea, vomiting, skin toxicity, neuropathy, anemia, hypersensitivity, alopecia high (days 1 and 8)   non–small cell paclitaxel–carboplatin– bevacizumab cisplatin–paclitaxel cisplatin–docetaxel cisplatin–gemcitabine cisplatin–vinorelbine– cetuximab cisplatin–vinorelbine carboplatin–paclitaxel gemcitabine–paclitaxel gemcitabine–docetaxel gemcitabine pemetrexed paclitaxel docetaxel small cell ep cav cisplatin–paclitaxel cisplatin–docetaxel cisplatin–gemcitabine cisplatin–vinorelbine– cetuximab cisplatin–vinorelbine carboplatin–paclitaxel gemcitabine–paclitaxel gemcitabine–docetaxel gemcitabine pemetrexed paclitaxel docetaxel high (day 2 only) high (day 1 only) high (day 1) mild (days 8/15) high (day 1 only) high (day 1 only) moderate moderate mild mild mild (day 1 only) mild (continued) 1340  section 16  |  oncologic disorders table 90–4  chemotherapy regimens in lung cancer and associated toxicities13,17,19,24,33–37 (continued) small cell ep cav ec ic topotecan   other significant toxicities infection, nausea, vomiting, thrombocytopenia, anemia nausea, vomiting, thrombocytopenia, neuropathy, hepatic, renal, alopecia infection, thrombocytopenia, alopecia fever, infection, thrombocytopenia, anemia, diarrhea, nausea and vomiting, elevated liver enzymes neutropenic fever, neutropenic sepsis, anemia, thrombocytopenia, nausea, fatigue, vomiting, stomatitis, anorexia, diarrhea, fever   nausea/vomiting potential high (day 2 only) high high (day 1 only) high (day 1), moderate (days 8/15) mild (days 1–5) auc, area under the curve. Cav, cyclophosphamide–doxorubicin–vincristine. Ec, etoposide–carboplatin. Ep, etoposide–cisplatin. Ic, irinotecan– cisplatin. Im, intramuscular. Iv, intravenous. See chapter 88 for dose reductions for hepatic and renal dysfunction. Cure, whereas surgery did not. 12 in the vast majority of patients, chemotherapy with or without radiotherapy is the treatment of choice. Even after a complete response to therapy, the cancer usually recurs within 6 to 8 months, and the survival time following recurrence is typically short (~ 4 months). This yields an average survival rate of 14 to 20 months for limited disease and 8 to 13 months for extensive disease.

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