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By: Ashley H. Vincent, PharmD, BCACP, BCPS
- Clinical Associate Professor, Department of Pharmacy Practice, College of Pharmacy, Purdue University, West Lafayette
- Clinical Pharmacy Specialist—Ambulatory Care, IU Health Physicians Adult Ambulatory Care Center, Indianapolis, Indiana
Etiology and Risk Factors Night shift workers may be at higher risk for delayed sleep phase syndrome due to antibiotics vs appendectomy order respidox 100 mg free shipping irregular circadian entrainment (Santhi et al antibiotic resistance patterns generic respidox 200 mg without prescription. Similarly inflection point cheap respidox 200 mg on-line, individuals who live in extreme latitudes and are exposed to antibiotic resistance food safety buy cheap respidox 100mg line extended periods of light may also be at increased risk of suffering from delayed sleep phase syndrome (Lingjaerde et al. Biological, physiological, and genetic factors have been proposed to be responsible for causing delayed sleep phase syndrome. Furthermore, exposure to dim light in the late evening and at night, may also affect the circadian phase (Zeitzer et al. Biological alterations to the endogenous circadian system also contribute to delayed sleep phase syndrome. Although levels of melatonin typically increase in the evening hours, individuals with this syndrome have a hypersensitivity to nighttime bright light exposure in the suppression of melatonin (Czeisler et al. It has also been hypothesized that the disorder may result from a circadian phase that has a reduced sensitivity to photic entrainment, or the free-running period of the circadian cycle is prolonged (Czeisler et al. Consistent with these hypotheses, polymorphisms in circadian genes influence the entraining and free-running period of the circadian cycle and may be associated with delayed sleep phase syndrome (Takahashi et al. Treatment Treatment for delayed sleep phase syndrome requires resynchronizing to a more appropriate phase to the 24-hour light-dark cycle. In addition to a structured sleep-wake schedule and good sleep hygiene practices, potential therapies include resetting the circadian pacemaker with bright light, melatonin, or a combination of both. However, studies that have investigated the efficacy of bright light have provided mixed results (Pelayo et al. Similarly, there have been no large-scale controlled studies examining the efficacy of melatonin, and as of yet it has not been approved by the Food and Drug Administration for this indication (Reid and Zee, 2005). Advanced Sleep Phase Syndrome Manifestations and Prevalence Advanced sleep phase syndrome (or advanced sleep phase type) is characterized by involuntary bedtimes and awake times that are more than 3 hours earlier than societal means (Figure 3-7) (Reid and Zee, 2005). As is the case with delayed sleep phase syndrome, the amount of sleep is not affected, unless evening activities result in later bedtimes. Therefore, the syndrome is primarily associated with impaired social and occupational activities. The prevalence of advanced sleep phase syndrome is unknown; however, it has been estimated that as many as 1 percent of the middle-aged adults may suffer from it (Ando et al. One of the challenges in determining its prevalence is that affected individuals typically do not perceive it as a disorder and therefore do not seek medical treatment (Reid and Zee, 2005). Etiology and Risk Factors the causes of this syndrome are not known; however, as with delayed sleep phase type, biological and environmental factors likely contribute to the onset of advanced sleep phase type. Polymorphisms in circadian clock genes have been identified in a family with advanced sleep phase syndrome (Toh et al. Changes in the activity of genes involved in circadian biology are consistent with observations that individuals with this syndrome have circadian rhythms that are less than 24 hours. Treatment Treatment options for individuals with advanced sleep phase syndrome are limited. Bright light therapy in the evening has been used successfully in a limited study to reduce awakenings (Campbell et al. Changing concepts of sudden infant death syndrome: Implications for infant sleeping environment and sleep position. Successful combined treatment with vitamin B12 and bright artificial light of one case with delayed sleep phase syndrome. The delayed sleep phase syndrome: Clinical and investigative findings in 14 subjects. The changing concept of sudden infant death syndrome: Diagnostic coding shifts, controversies regarding the sleeping environment, and new variables to consider in reducing risk. Twenty-four-hour ambulatory blood pressure in children with sleep-disordered breathing. Morbidity, mortality and sleep-disordered breathing in community dwelling elderly. Kindling antagonism: Effects of norepinephrine depletion on kindled seizure suppression after concurrent, alternate stimulation in rats.
Clinical evidence In a study in 14 healthy subjects virus upper respiratory cheap respidox 200 mg on-line, ginkgo 120 mg twice daily for 2 weeks had no significant effect on the pharmacokinetics of lopinavir/ritonavir 400 mg/100 mg twice daily (given for 2 weeks alone before adding the ginkgo) bacteria experiments buy generic respidox 200 mg. The ginkgo extract was assayed and contained 29% flavonol glycosides and 5% terpene lactones treatment for dogs dermatitis cheap respidox 100mg without a prescription. Importance and management the study here shows that ginkgo does not alter the pharmacokinetics of lopinavir/ritonavir infection 3 months after miscarriage generic respidox 100 mg line, and no special precautions are required on concurrent use. As regards protease inhibitors that are not boosted by ritonavir, the authors of this study recommend avoiding ginkgo. Ginkgo + Risperidone An isolated case describes priapism in a patient taking risperidone and ginkgo. Clinical evidence A 26-year-old paranoid schizophrenic who had been taking risperidone 3 mg daily for the past 3 years developed priapism that had lasted for 4 hours 2 weeks after starting ginkgo 160 mg daily for occasional tinnitus. Risperidone was then restarted and the patient reported no further episodes of priapism at follow-up 6 months later. Risperidone alone does rarely cause priapism, probably because of its alpha-adrenergic properties, and ginkgo might have vascular effects that could be additive. Importance and management the use of ginkgo is widespread and this appears to be the only report in the literature of an interaction with risperidone. G Clinical evidence In one study, 18 healthy Chinese subjects were given a single 40-mg dose of omeprazole before and after a 12-day course of a standardised extract of ginkgo 140 mg twice daily. Importance and management this appears to be the only study examining the effects of ginkgo on proton pump inhibitors. Pharmacogenetics and herb-drug interactions: experience with Ginkgo biloba and omeprazole. Ginkgo + Theophylline the interaction between ginkgo and theophylline is based on experimental evidence only. Importance and management the evidence for this interaction is limited to experimental data and the dose of ginkgo used is far higher than the most common clinical dose. Therefore an interaction with theophylline based on this mechanism is unlikely to be clinically important. Herb-drug interactions: Effect of Ginkgo biloba extract on the pharmacokinetics of theophylline in rats. Mechanism It was suggested that the flavonoids in the ginkgo had a subclinical direct effect on the benzodiazepine receptor. Importance and management Evidence for an interaction between ginkgo and trazodone appears to be limited to this isolated case, from which no general conclusions can be drawn. Bear this interaction in mind in case of an unexpected response to concurrent use. Ginkgo + Tolbutamide Gingko does not appear to have a clinically relevant effect on the metabolism or blood-glucose-lowering effects of tolbutamide. Clinical evidence In healthy subjects, ginkgo extract (Ginkgold) 120 mg twice daily for 7 days had no effect on the urinary metabolic ratio of tolbutamide. The ginkgo product used was Ginkgold, which contained 24% flavone glycosides and 6% terpene lactones. The pharmacodynamics of tolbutamide were not significantly altered although there was a tendency towards the attenuation of its hypoglycaemic effects by ginkgo (14% reduction). However, when a single 100-mg/kg dose of ginkgo was given with a single 40-mg/kg dose of tolbutamide, the blood-glucose levels were significantly lower, when compared with tolbutamide alone, suggesting that ginkgo potentiated the blood-glucose-lowering effects of tolbutamide. The disparate effects between single and multiple dose administration in the animal study are not understood. Importance and management From the clinical evidence, it is clear that ginkgo has little, if any, effect on the metabolism and blood-glucose-lowering effects of tolbutamide. Effects of Ginkgo biloba extract on pharmacokinetics and pharmacodynamics of tolbutamide and midazolam in healthy volunteers. Ginkgo biloba extract modifies hypoglycemic action of tolbutamide via hepatic cytochrome P450 mediated mechanism in aged rats. Ginkgo + Warfarin and related drugs Evidence from pharmacological studies in patients and healthy subjects suggests that ginkgo does not usually interact with warfarin. However, an isolated report describes intracerebral haemorrhage associated with the use of ginkgo and warfarin, and there are a few reports of bleeding associated with the use of ginkgo alone.
In addition bacteria water test kit discount respidox 200mg overnight delivery, the incidence and severity of headaches antibiotic resistance evolves in bacteria when discount 100 mg respidox with mastercard, hot flushes and dizziness tended to antibiotic 8 months baby cheap respidox 100mg on line be higher with the combination when compared with nifedipine alone antibiotics for severe acne generic respidox 200 mg. Subjects also experienced increased heart rate with the combination although the decrease in blood pressure was unaffected. Mechanism Experimental data3 have found that ginkgo has no significant effect on the pharmacokinetics of intravenous nifedipine, suggesting that ginkgo reduces the first-pass metabolism of nifedipine. Ginkgo Importance and management the evidence for an interaction between ginkgo and ciclosporin is limited to one study in rats. However, ginkgo contains flavonoids, and of these quercetin has been implicated in modest interactions with ciclosporin in other studies (see Flavonoids + Ciclosporin, page 190 for more information). On this basis, while there is insufficient evidence to suggest that concurrent use should be avoided, there is the possibility that ginkgo may make ciclosporin levels less stable as the quercetin content of different preparations is likely to vary. Clinical evidence A study in 8 healthy subjects found that ginkgo leaf extract 80 mg three times daily had no significant effects on the pharmacokinetics of a single 500-microgram dose of digoxin. Importance and management the clinical study suggests that ginkgo is unlikely to alter digoxin levels in clinical use. Therefore no dosage adjustment would be expected to be necessary if patients taking digoxin also wish to take ginkgo. As digoxin is used as a probe substrate for P-glycoprotein, this study also suggests that ginkgo is unlikely to interact with other drugs that are substrates of P-glycoprotein. Ginkgo + Dextromethorphan Ginkgo does not appear to affect the metabolism of dextromethorphan. Clinical evidence Ginkgo leaf extract 120 mg twice daily for 16 days was given to 12 healthy subjects with a single 30-mg dose of dextromethorphan on day 14. The ginkgo preparation (Ginkgold) contained ginkgo flavonol glycosides 24% and terpene lactones 6%. There was no change in the metabolism of dextromethorphan when it was taken after the ginkgo. Importance and management the available evidence seems to reliably suggest that ginkgo does not affect the pharmacokinetics of dextromethorphan. G Ginkgo + Donepezil Ginkgo does not appear to alter the pharmacokinetics or effects of donepezil. Concurrent use did not affect the pharmacokinetics or cholinesterase activity of donepezil, and cognitive function appeared to be unchanged. The effects of Ginkgo biloba extracts on the pharmacokinetics and pharmacodynamics of donepezil. Ginkgo + Fexofenadine Ginkgo does not appear to affect the pharmacokinetics of fexofenadine. Evidence, mechanism, importance and management In a clinical study, 13 healthy subjects took a single oral dose of fexofenadine 120 mg after 4 weeks of twice-daily doses of ginkgo 120 mg containing 29% flavonol glycosides and 5% terpene lactones. Over the next couple of days she exhibited a variety of psychotic symptoms including paranoid delusions, disorganised behaviour, anxiety and auditory hallucinations. Her blood-alcohol level was zero on admission and there was no evidence of alcohol withdrawal during her stay in hospital. Fexofenadine is a P-glycoprotein substrate and the findings of this study therefore suggest that ginkgo does not affect P-glycoprotein activity. These factors make it difficult to find the exact cause of the psychotic symptoms. Importance and management this appears to be the only case report in the literature and, because of the multiple factors involved, such as a history of alcohol abuse, it is difficult to assess its general importance. Bear this interaction in mind in case of an adverse response to the combination of ginkgo and valerian. Ginkgo + Haloperidol Animal studies suggest that ginkgo may increase extrapyramidal effects in response to haloperidol, but clinical studies do not appear to have reported this effect. Clinical evidence Ginkgo has been tried in schizophrenia as an addition to standard antipsychotics such as haloperidol. For example, in one clinical study, an improvement in positive symptoms was seen in 43 schizophrenic patients given ginkgo extract 360 mg daily with haloperidol 250 micrograms/kg daily for 12 weeks. It is thought that ginkgo may interfere with dopamine neurotransmission by scavenging nitric oxide, which in turn reduces locomotor activity. Importance and management the authors of the experimental study caution that there is a possibility of an increase in extrapyramidal effects when ginkgo is used with haloperidol.
Oral bioavailability is good infection 2 tips respidox 100mg on-line, but absorption is decreased by 20% to do they give antibiotics for sinus infection discount respidox 100 mg online 30% by food bacteria prokaryotes purchase respidox 100mg with amex, especially milk antibiotics for uti in cats discount respidox 200 mg visa. Sotalol does not bind to plasma proteins, is not metabolized, and is renally excreted as unchanged drug. Special Considerations/Preparation Oral formulation supplied in 80-mg, 120-mg, 160-mg, and 240-mg tablets. Potassium supplementation and potassium rich diets are not recommended with spironolactone use. Metabolized to canrenone and 7-a-thiomethylspironolactone, active metabolites with extended elimination half-lives. Monitoring 782 Micormedex NeoFax Essentials 2014 Follow serum potassium closely during long-term therapy. To prepare 25 mg/mL oral suspension, grind one hundred twenty (120) 25-mg tablets to a fine powder in a mortar. Suspension is stable for 60 days refrigerated or at room temperature (at 5 and 25 degrees C). Karim A: Spironolactone: Disposition, metabolism, pharmacodynamics, and bioavailability. Transfer contents of the mortar to the calibrated bottle and add enough vehicle to bring the total volume to 120 mL. Terai I, Yamano K, Ichihara N, et al: Influence of spironolactone on neonatal screening for congenital adrenal hyperplasia. Premedication is recommended in neonates for all non-emergent intubations if time permits. Premedication regimens for endotracheal intubation typically include a skeletal muscle relaxant in combination with an analgesic (an opioid) and/or sedative and a vagolytic agent (usually atropine)     . Premedication has been shown to decrease the time to successful intubation and decrease the occurrence of adverse effects (ie, increased intracranial pressure, hypertension, decreased heart rate and oxygenation) in neonates     . Use of succinylcholine has resulted in fewer intubation attempts and more successful intubations compared with no succinylcholine in clinical studies in neonates . Contraindications/Precautions Contraindicated in the acute phase of injury after multiple trauma, major burns, extensive denervation of skeletal muscle, or upper motor neuron injury; may result in severe hyperkalemia, and possible onset of cardiac arrest. Also contraindicated in patients with a personal or family history of malignant hyperthermia and in patients with skeletal muscle myopathies . Intragastric pressure increase may occur, resulting in regurgitation and possible aspiration of stomach contents. Initial muscle fasciculations may cause additional trauma in patients with fractures or muscle spasm . This syndrome often presents as peaked T-waves and sudden cardiac arrest within minutes after the administration of the drug. If there are signs present for malignant hyperthermia, appropriate treatment should be instituted concurrently. Pharmacology Succinylcholine is an ultra short-acting depolarizing-type, skeletal muscle relaxant. Adverse Effects Hypertension, hypotension, prolonged respiratory depression or apnea, jaw rigidity, postoperative muscle pain, excessive salivation, and rash have been reported . Monitor temperature and 787 Micormedex NeoFax Essentials 2014 expired carbon dioxide continuously for early recognition of malignant hyperthermia . Carbajal R: Premedication for tracheal intubation in neonates: confusion or controversy? Repeat doses of 1 mg/kg up to a maximum total dose of 4 mg/kg have been used if muscle relaxation was not attained by 1 to 3 minutes after administration  . Uses Skeletal muscle relaxation/paralysis for neonates requiring rapid sequence intubation or non-emergent endotracheal intubation          . Bradycardia and possible asystole may occur; higher risk with second dose; incidence and severity increased in pediatric patients compared with adults; premedication regimen that includes atropine may protect against bradyarrhythmias induced by succinylcholine. Serious cardiac arrhythmias or cardiac arrest due to hyperkalemia may occur in patients with massive digitalis toxicity or patients with electrolyte abnormalities.
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