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essay on psychological disorders Vascular imaging is particularly important in sickle cell disease due to the risk or vasculopathy and concomitant moyamoya. Rans usion, particularly exchange trans usion, should be strongly considered given its immediate bene t in reducing the burden o sickle hemoglobin. A typical goal is to reduce hbs concentration to < 30%. In addition to trans usion therapy, thrombolytics and aspirin can be used e ectively in the appropriate clinical circumstances.2,4 what are other red blood cell disorders for neurologists to consider in the inpatient setting?. Anemia due to nutritional de iciencies or toxins—b12, lead poisoning structural abnormalities—hereditary spherocytosis, neuroacanthocytosis int er nal medic ine and neur ology disorders o production—aplastic anemia, polycythemia vera (pv) disorders o destruction—autoimmune hemolytic anemia, microangiopathic hemolytic anemia associated with autoimmune disease or platelet disorders (see part 1.2) how are nutritional deficiencies identified?. T e complete blood count and peripheral blood smear are help ul in initial laboratory studies or the identi cation o nutritional de ciencies associated with hematologic abnormalities (see figure 51-1). Based on the combination o clinical suspicion (eg, dorsal column dys unction) and suggestive abnormalities (eg, hypersegmented neutrophils with macrocytic anemia), more speci c testing (eg, vitamin b12, methylmalonic acid, and homocysteine levels) can help to arrive at the appropriate diagnosis (eg, b12 de ciency). How are nutritional or toxin-induced red cell disorders treated?. O en, replacement o the de cient product or removal o the o ending agent will correct the associated abnormalities. Even in the hospital setting, repletion can be guided by evidence-based literature to ensure sa e, e ective, and ef cient delivery o care. O continue the example illustrated above, a 2005 cochrane review ound that high oral doses o vitamin b12 could achieve hematologic and neurologic responses as e ectively as intramuscular administration.5 un ortunately, not all hematologic disorders are as common and readily diagnosed as nutritional de ciencies. 847 what other red blood cell findings could suggest an underlying disorder with neurological consequences?. One important, but rare, cause o neurologic dys unction associated with hematologic abnormality is the group o genetic neurodegenerative diseases re erred to as neuroacanthocytosis. In addition to the presence o characteristic spiky red blood cells, known as acanthocytes, on peripheral smear, these diseases include eatures such as dystonia, chorea, and neurodegeneration o the basal ganglia. Current classi cation o neuroacanthocytosis consists o 4 subtypes. Chorea-acanthocytosis, mcleod syndrome, huntington disease-like 2, and pantothenate kinase-associated neurodegeneration.6 when should neuroacanthocytosis be suspected?. Patients exhibiting the signs and symptoms o a movement disorder with negative testing or huntington disease and suggestive neuroimaging ndings, such as iron deposition in the basal ganglia, should be considered or this disease, particularly i acanthocytes are identi ed on peripheral blood smear. Genetic testing can both con rm the diagnosis and distinguish the various subtypes. What are the treatment options for neuroacanthocytosis?. As the role o acanthocytes in the neurologic mani estations o neuroacanthocytosis is unclear, numerous medical therapies directed at alleviating symptoms—botulinum toxin a, tetrabenazine, and atypical neuroleptics, or example—have produced disappointing long-term results. More aggressive interventions may hold promise but must be undertaken care ully and with expert consultation. A case report by lim et al7 described marked improvement in dystonia, chorea, and overall quality o li e in a 32-year-old patient who underwent deep brain stimulation (dbs) but only a er a ailed rst attempt due to intraoperative complications. Are there conditions where the red blood cell disorder causes both direct and indirect neurological manifestations?. ▲ figure 51-1 hypersegmented neutrophils in vitamin b12 de ciency. Reproduced with permission from soupir cp and hasserjian rp. Myeloid neoplasms and mastocytosis. Therapy-related myeloid neoplasm session from the 2007 workshop of society for hematopathology and european association for haematopathology. Pv is a condition classi ed as a myeloproli erative disorder where myeloid expansion in the peripheral blood leads to excessive numbers o circulating red blood cells (see table 51-1). Interestingly, while the hyperviscosity o pv carries its own neurological risks, hemorrhage and thrombosis alone do not decisively explain all neurologic symptoms associated with the disease. How is pv diagnosed?.

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http://manila.lpu.edu.ph/about.php?test=help-i-can-do-my-homework help i can do my homework Vd can be cialis drug screen calculated as follows. Vd = 0. 7 l/kg x dw (in kg). A ld can then be calculated using vd and a target concentration. Ld = ctarget x vd. Fosphenytoin  fosphenytoin is a water-soluble, phosphoester prodrug that is rapidly converted to phenytoin in the body. It is compatible with most iv solutions. It is dosed in phenytoin equivalents (pe), and it can be infused up to 150 mg pe/minute. Although it has fewer cardiovascular side effects than phenytoin, clinicians should continuously monitor blood pressure, ecg, and heart rate. Maintenance doses can be started 12 hours after the ld. Paresthesias, especially around the lips and groin are common, but typically resolve within a few minutes and should not necessitate stopping the infusion. If a postload serum level is desired, it should be obtained 2 hours after an iv load. Phenobarbital  if phenytoin or fosphenytoin fails to prevent seizure recurrence, phenobarbital can be considered. However, emerging evidence suggests that phenobarbital may not be effective if se persists despite benzodiazepines and phenytoin. This may be due to progressive resistance of the gabaa receptor, where barbiturates also act. 20 adverse reactions of phenobarbital include sedation, hypotension, and respiratory depression. Therefore, patients receiving a rapid iv ld of phenobarbital should have hemodynamic monitoring and be mechanically ventilated if at high risk of respiratory compromise. Its long half-life makes it a popular agent for both acute treatment and chronic maintenance therapy or as adjunct therapy to prevent withdrawal seizures when weaning refractory se patients off pentobarbital infusions. Valproate sodium although valproate sodium is not food and drug administration (fda)-approved for se, it has been used iv in various types of se including generalized tonic-clonic, myoclonic, and ncse. 21 it is particularly useful in patients with chapter 32  |  status epilepticus  501 table 32–1  medications used in adult status epilepticus drug name (brand name) diazepam (valium) lorazepam (ativan) midazolam (versed) phenytoin (dilantin) loading dose and rse maintenance dose (if applicable) administration rate 0. 15 mg/kg (up to 10 mg 5 mg/min (ivp) per dose). May repeat in 5 minutes 0. 1 mg/kg (up to 4 mg per 2 mg/min (ivp) dose). Repeat in 5–10 minutes 0. 2 mg/kg im up to 10 mg per dose rse. 0.

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what is a good argumentative essay topic Ototoxicity is a wellestablished side effect of furosemide and ethacrynic acid that occurs rarely with bumetanide and torsemide. For furosemide, the risk of ototoxicity is greater when administered by the iv route at a rate exceeding 4 mg/min. The incidence of ototoxicity is higher for ethacrynic acid compared with the other loop diuretics. However, ethacrynic acid is the only loop diuretic that does not contain a sulfonamide moiety and its use has been recommended in individuals with a sulfa allergy. However, there is very weak evidence of crossallergenicity between sulfa-containing antibiotics and diuretics. 18 with its high incidence of ototoxicity, ethacrynic acid is not recommended. There are several pharmacokinetic differences among loop diuretics. About 85% of furosemide is excreted unchanged by the kidney. 19 in contrast, liver metabolism accounts for 50% and 80% of the elimination of bumetanide and torsemide, respectively. 19 the bioavailability of both torsemide and bumetanide is higher than for furosemide with an iv-to-oral ratio of 1:1. The bioavailability of oral furosemide is approximately 50% to 65%. 20 thus, the iv-to-oral ratio for furosemide is about 1:2. The pharmacodynamic characteristics of loop diuretics are similar when equivalent doses are administered. Loop diuretics exert their effect from the luminal (urinary) side of the tubule. Substances that interfere with the secretion of loop diuretics, such as endogenous organic acids that accumulate in kidney disease, competitively inhibit secretion of loop diuretics into the lumen of the tubules. Therefore, large doses of loop diuretics are often necessary in kidney disease to ensure that adequate drug reaches the nephron lumen.

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