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http://cs.gmu.edu/~xzhou10/semester/proofreading-strategies.html proofreading strategies Pharmacologic approaches to treatment treatment of ahf targets relief of congestion and optimization of co utilizing oral or iv diuretics, iv vasodilators, and, when appropriate, inotropes based on presenting hemodynamics. Current treatment strategies in ahf target improving hemodynamics while preserving organ function. A specific treatment approach is formulated depending on the patient’s symptoms (congestion versus hypoperfusion) and hemodynamic indices (ci and pcwp). 40 if the patient primarily exhibits signs and symptoms of congestion, treatment entails use of diuretics as first-line agents to decrease pcwp. Additionally, iv vasodilators are added to provide rapid relief of congestion and additional reductions in pcwp. By reducing congestion in the heart, cardiac contractile function may improve, which results in an increase in sv and co, and hence perfusion to vital organs. The patient’s presenting bp can also help guide the clinician on choice of diuretic, vasodilator, or both.

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canadian history thesis topics Studies in the 1990s found that hydroxyurea increases hbf levels as well as increasing the number of hbf-containing reticulocytes and intracellular hbf. Other beneficial effects of hydroxyurea include antioxidant properties, reduction of neutrophils and monocytes, increased intracellular water content leading to increased red cell deformability, decreased red cell adhesion to endothelium, and increased levels of nitric oxide, which is a regulator involved in physiologic disturbances. 16 hydroxyurea reduced the frequency of hospitalizations and the incidences of pain, acute chest syndrome (acs), and blood transfusions by almost 50% in a landmark trial in adult scd patients with moderate to severe disease. Hemoglobin and hbf concentrations increased and hemolysis decreased. 16 a follow-up study demonstrated a 40% reduction in mortality over a 9-year period in patients continuing to receive hydroxyurea. 17 not all patients responded equally. Therefore, hydroxyurea may not be the best option for all patients. The use of hydroxyurea in children and adolescents with scd has been investigated, and similar results were reported as in adult trials, with no adverse effects on growth and development. 4,18,19 hydroxyurea is recommended as an option for children with moderate to severe scd. 20 the most common adverse effect of hydroxyurea is myelosuppression. Long-term adverse effects are unknown, but myelodysplasia, acute leukemia, and chronic opportunistic infections have been reported. 16 hydroxyurea is teratogenic in high doses in animal studies and this is a concern, which should be addressed with patients. Normal pregnancies with no birth defects have been reported in some women receiving hydroxyurea, but close monitoring and weighing risk versus benefit to the patient are vitally important. Hydroxyurea is excreted in breast milk and should be avoided in lactating mothers. 16 hydroxyurea should be considered in scd with frequent vasoocclusive crises, severe symptomatic anemia, repeated history of acs, or other history of severe vasoocclusive crisis (voc) complications. 4 the prevention of organ damage or reversal of previous damage has not been shown to occur with chronic use of hydroxyurea. 17 the goals of therapy with hydroxyurea are to decrease the acute complications of scd, improve quality of life, and reduce the number and severity of pain crises. Hydroxyurea is available in 200-, 300-, 400-, and 500-mg capsules. Extemporaneous liquid preparations can be prepared for children who cannot swallow capsules. Doses should start at 10 to 15 mg/kg daily in a single oral dose, which can be increased after 8 to 12 weeks if blood counts are stable and there are no side effects. Individualize the dosage based on the patient’s response and the toxicity seen. With close monitoring, doses can be increased 5 mg/kg/day up to 35 mg/kg daily. 16 in patients with renal failure, dosing of hydroxyurea will need to be adjusted according to the creatinine clearance, as shown in table 68–3.

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help me write my book report 4,9,20 the degree of iridotrabecular contact (angle closure) can be assessed by visualizing the anatomy of the irido-corneal angle by gonioscopy. Clinical presentation and diagnosis risk factor evaluation for poag, only 4% to 8% of patients may progress to legal blindness. Vision loss does not occur until there has been significant loss of the retinal ganglion cells. It may take 13 to 16 years for a patient to go blind from glaucoma. A patient’s quality of life may not be affected until significant visual field loss is present and the patient can no longer perform the activities of daily living. 21 practitioners can play an important role in eye care by assessing patients for risk factors and referring to an eye care specialist for appropriate screening and evaluation. Risk factor evaluation is essential in determining the frequency of comprehensive eye examinations for patients (table 61–2). Table 61–3  risk factors for glaucoma poag pacg elevated iop african or hispanic descent family history of glaucoma older age thinner cct type 2 diabetes low ocular perfusion pressures myopia advancing age asian or eskimo ethnicity female sex hyperopia shallow anterior chamber family history of angle-closure glaucoma   cct, central corneal thickness. Iop, intraocular pressure. Pacg, primary angle-closure glaucoma. Poag, primary open-angle glaucoma. Data from refs. 3 and 4. Glaucoma risk factors are also useful in deciding when to start therapy and determining the sequence of pharmacotherapeutic or surgical treatment modalities. 2–4 table 61–3 lists the major risk factors associated with poag and pacg. The development of pacg is associated with several anatomical risk factors that lead to shallow anterior chambers. Pacg patients may have a thick, anteriorly displaced lens that results from continued growth of the lens and/or cataractous changes. The anterior chamber depth is typically shallower in many individuals with pacg, which predisposes these eyes to anatomically narrower iridocorneal inlets that are a setup for developing critically narrow angles more susceptible to closure (from an enlarging cataractous lens or other insults). 4,20 patients with pacg are characterized by at least 180 degrees of iridotrabecular contact, elevated iop, and ophthalmic examination characteristic of glaucomatous changes. Recurrent attacks or a prolonged acute attack can lead to the development of peripheral anterior synechia, which partially obstructs the flow of aqueous humor through the trabecular meshwork. 4,20 clinical presentation and diagnosis of poag general •• adult onset (usually greater than 40 years of age) •• patients may be unaware that they have glaucoma and may be diagnosed during routine eye evaluation •• poag is usually bilateral with asymmetric disease progression symptoms •• patients with severe disease progression may report loss of peripheral vision (“tunnel vision”) and may describe the presence of paracentral, nasal, and arcuate scotoma (blind spots) in their field of vision signs •• ophthalmoscopic examination may reveal. •• optic nerve head (optic disc) cupping •• large cup-to-disc ratio •• diffuse thinning, focal narrowing, or notching of the optic nerve head rim •• splinter hemorrhages •• optic nerve head/nerve fiber layer changes occur before visual field changes can be detected diagnostic tests •• gonioscopy—anterior-chamber angles are to be open •• applanation tonometry—elevated iop (greater than 21 mm hg [2. 8 kpa]) may be present. However, patient can have signs of optic neuropathy without elevated iop •• pachymetry—measures central corneal thickness. Thin corneas (less than 540 μm) are considered a glaucoma risk factor •• automated static threshold perimetry—evaluates visual fields. Can detect defects in the visual field before a patient may notice •• other diagnostic tests—scanning laser polarimetry, confocal scanning laser ophthalmoscopy, and optical coherence tomography chapter 61  |  glaucoma  925 clinical presentation and diagnosis of acute angle-closure crisis general •• medical emergency due to high risk of vision loss •• unilateral in presentation, but fellow eye is at risk symptoms •• ocular pain •• red eye •• blurry vision •• halos around lights •• systemic symptoms may develop. •• nausea/vomiting •• abdominal pain •• headache •• diaphoresis treatment primary open-angle glaucoma »» desired outcomes and goals the goals of therapy are to prevent further loss of visual function. Minimize adverse effects of therapy and impact on the patient’s vision, general health, and quality of life. Maintain iop at or below a pressure at which further optic nerve damage is unlikely to occur. And educate and involve the patient in the management of their disease. Current therapy is directed at altering the flow and production of aqueous humor, which is the major determinant of iop.

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http://projects.csail.mit.edu/courseware/?term=essay-ideas-for-middle-school essay ideas for middle school Early electrodiagnostic indings in guillain-barré syndrome. Arch neurol. Jun 2001;58(6):913-917. 7. Derksen a, ritter c, athar p, et al. Sural sparing pattern discriminates guillain-barré syndrome rom its mimics. Muscle nerve. Nov 2014;50(5):780-784. 8. Hiraga a, kuwabara s, ogawara k, et al. Patterns and serial changes in electrodiagnostic abnormalities o axonal guillainbarré syndrome. Neurology. Mar 8 2005;64(5):856-860. 9. Kaida k, morita d, kanzaki m, et al.

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