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hyvee inc - piperonyl butoxide (unii: lwk91tu9ah) (piperonyl butoxide - unii:lwk91tu9ah) - piperonyl butoxide 4 g in 100 ml

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mckesson - piperonyl butoxide (unii: lwk91tu9ah) (piperonyl butoxide - unii:lwk91tu9ah) - piperonyl butoxide 4 ml in 100 ml

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target corporation - piperonyl butoxide 4%, pyrethrum extract (equivalent to 0.33% pyrethrins) -

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cvs pharmacy - piperonyl butoxide 4%, pyrethrum extract (equivalent to 0.33% pyrethrins) -

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rising pharma holdings, inc. - rizatriptan benzoate (unii: wr978s7qhh) (rizatriptan - unii:51086hbw8g) - rizatriptan 5 mg - rizatriptan benzoate tablets are indicated for the acute treatment of migraine with or without aura in adults and in pediatric patients 6 to 17 years old. limitations of use - rizatriptan benzoate tablets should only be used where a clear diagnosis of migraine has been established. if a patient has no response for the first migraine attack treated with rizatriptan benzoate tablets, the diagnosis of migraine should be reconsidered before rizatriptan benzoate tablets are administered to treat any subsequent attacks. - rizatriptan benzoate tablets are not indicated for use in the management of hemiplegic or basilar migraine [see contraindications (4)] . - rizatriptan benzoate tablets are not indicated for the prevention of migraine attacks. - safety and effectiveness of rizatriptan benzoate tablets have not been established for cluster headache. rizatriptan benzoate tablets are contraindicated in patients with: - ischemic coronary artery disease (angina pectoris, history of myocardial infarction, or documented silent ischemia), or other significant underlying cardiovascular disease [see warnings and precautions (5.1)] . - coronary artery vasospasm including prinzmetal's angina [see warnings and precautions (5.1) ] . - history of stroke or transient ischemic attack (tia) [s ee warnings and precautions (5.4) ] . - peripheral vascular disease (pvd) [see warnings and precautions (5.5) ] . - ischemic bowel disease [see warnings and precautions (5.5) ] . - uncontrolled hypertension [see warnings and precautions (5.8) ] . - recent use (i.e., within 24 hours) of another 5-ht1 agonist, ergotamine-containing medication, or ergot-type medication (such as dihydroergotamine or methysergide) [see drug interactions (7.2 and 7.3) ] . - hemiplegic or basilar migraine [see indications and usage (1) ]. - concurrent administration or recent discontinuation (i.e., within 2 weeks) of a mao-a inhibitor [see drug interactions (7.5) and clinical pharmacology (12.3) ] . - hypersensitivity to rizatriptan or any of the excipients (angioedema and anaphylaxis seen) [see adverse reactions (6.2) ] . risk summary available human data on the use of rizatriptan benzoate in pregnant women are not sufficient to draw conclusions about drug-associated risk for major birth defects and miscarriage. in animal studies, developmental toxicity was observed following oral administration of rizatriptan during pregnancy (decreased fetal body weight in rats) or throughout pregnancy and lactation (increased mortality, decreased body weight, and neurobehavioral impairment in rat offspring) at maternal plasma exposures greater than that expected at therapeutic doses in humans [see animal data]. in the u.s. general population, the estimated background risk of major birth defects and of miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. the reported rate of major birth defects among deliveries to women with migraine range from 2.2% to 2.9% and the reported rate of miscarriage was 17%, which are similar to rates reported in women without migraine. clinical considerations disease-associated maternal and/or embryo/fetal risk in women with migraine, there is an increased risk of adverse perinatal outcomes in the mother, including pre-eclampsia and gestational hypertension. data human data the pregnancy registry for rizatriptan benzoate did not identify any pattern of congenital anomalies or other adverse birth outcomes over the period of 1998 to 2018. however, the lack of identification of any pattern should be viewed with caution, as the number of prospective reports with outcome information was low and did not provide sufficient power to detect an increased risk of individual birth defects associated with the use of rizatriptan benzoate. additionally, there was significant loss to follow-up in the prospective pregnancy reports, further complicating this assessment of an association between rizatriptan benzoate and any pattern of congenital anomalies or other adverse birth outcomes. in a study using data from the swedish medical birth register, live births to women who reported using triptans or ergots during pregnancy were compared with those of women who did not. of the 157 births with first-trimester exposure to rizatriptan, 7 infants were born with malformations (relative risk 1.01 [95% ci: 0.40 to 2.08]). a study using linked data from the medical birth registry of norway to the norwegian prescription database compared pregnancy outcomes in women who redeemed prescriptions for triptans during pregnancy, as well as a migraine disease comparison group who redeemed prescriptions for triptans before pregnancy only, compared with a population control group. of the 310 women who redeemed prescriptions for rizatriptan during the first trimester, 10 had infants with major congenital malformations (or 1.03 [95% ci: 0.55 to 1.93]), while for the 271 women who redeemed prescriptions for rizatriptan before, but not during, pregnancy, 12 had infants with major congenital malformations (or 1.48 [95% ci: 0.83 to 2.64]), each compared with the population comparison group. animal data when rizatriptan (0, 2, 10, or 100 mg/kg/day) was administered orally to pregnant rats throughout organogenesis, a decrease in fetal body weight was observed at the highest doses tested. at the mid dose (10 mg/kg/day), which was a no-effect dose for adverse effects on embryofetal development, plasma exposure (auc) was approximately 15 times that in humans at the maximum recommended human dose (mrhd) of 30 mg/day. when rizatriptan (0, 5, 10, or 50 mg/kg/day) was administered orally to pregnant rabbits throughout organogenesis, no adverse fetal effects were observed. plasma exposure (auc) at the highest dose tested was 115 times that in humans at the mrhd. placental transfer of drug to the fetus was demonstrated in both species. oral administration of rizatriptan (0, 2, 10, or 100 mg/kg/day) to female rats prior to and during mating and continuing throughout gestation and lactation resulted in reduced body weight in offspring from birth and throughout lactation at all but the lowest dose tested (2 mg/kg/day). plasma exposure (auc) at the no-effect dose (2 mg/kg/day) for adverse effects on postnatal development was similar to that in humans at the mrhd. oral administration of rizatriptan (0, 5, 100, or 250 mg/kg/day) throughout organogenesis and lactation resulted in neonatal mortality, reduced body weight (which persisted into adulthood), and impaired neurobehavioral function in offspring at all but the lowest dose tested. plasma exposure (auc) at the no-effect dose for adverse effects on postnatal development (5 mg/kg/day) was approximately 8 times that in humans at the mrhd. risk summary there are no data on the presence of rizatriptan or any active metabolites in human milk, or on the effects of rizatriptan on the breastfed infant, or on milk production. rizatriptan was excreted in rat milk, with levels in milk approximately 6 times those in maternal plasma. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for rizatriptan benzoate and any potential adverse effects on the breastfed infant from rizatriptan benzoate or from the underlying maternal condition. data following oral administration of rizatriptan to lactating rats at a dose of 100 mg/kg/day, drug  concentrations of rizatriptan in milk samples exceeded maternal plasma drug concentrations by approximately 6-fold. safety and effectiveness in pediatric patients under 6 years of age have not been established. the efficacy and safety of rizatriptan benzoate in the acute treatment of migraine in patients aged 6 to 17 years was established in an adequate and well-controlled study [see clinical studies (14.2)] . the incidence of adverse reactions reported for pediatric patients in the acute clinical trial was similar in patients who received rizatriptan benzoate to those who received placebo. the adverse reaction pattern in pediatric patients is expected to be similar to that in adults. clinical studies of rizatriptan benzoate did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. other reported clinical experience has not identified differences in responses between the elderly and younger patients.  although the pharmacokinetics of rizatriptan were similar in elderly (aged ≥65 years) and in younger adults (n=17), in general, dose selection for an elderly patient should be cautious, starting at the low end of the dosing range. this reflects the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy. geriatric patients who have other cardiovascular risk factors (e.g., diabetes, hypertension, smoking, obesity, strong family history of coronary artery disease) should have a cardiovascular evaluation prior to receiving rizatriptan benzoate [see warnings and precautions (5.1)] .

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pfizer laboratories div pfizer inc - celecoxib (unii: jcx84q7j1l) (celecoxib - unii:jcx84q7j1l) - celecoxib 50 mg - celebrex is indicated for the management of the signs and symptoms of oa [see clinical studies (14.1) ]. for the management of the signs and symptoms of ra [see clinical studies (14.2) ]. for the management of the signs and symptoms of jra in patients 2 years and older [see clinical studies (14.3) ]. for the management of the signs and symptoms of as [see clinical studies (14.4) ]. for the management of acute pain in adults [see clinical studies (14.5) ]. for the management of primary dysmenorrhea [see clinical studies (14.5) ]. celebrex is contraindicated in the following patients: risk summary use of nsaids, including celebrex, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of celebrex use between about 20 and 30 weeks of gestation and avoid celebrex use at about 30 weeks of gestation and later in pregnancy (see error! hyperlink reference not valid. , error! hyperlink reference not valid. ). premature closure of fetal ductus arteriosus use of nsaids, including celebrex, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding other potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in animal reproduction studies, embryo-fetal deaths and an increase in diaphragmatic hernias were observed in rats administered celecoxib daily during the period of organogenesis at oral doses approximately 6 times the maximum recommended human dose (mrhd) of 200 mg twice daily. in addition, structural abnormalities (e.g., septal defects, ribs fused, sternebrae fused and sternebrae misshapen) were observed in rabbits given daily oral doses of celecoxib during the period of organogenesis at approximately 2 times the mrhd (see error! hyperlink reference not valid. ). based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as celecoxib, resulted in increased pre- and post-implantation loss. prostaglandins also have been shown to have an important role in fetal kidney development. in published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses. the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations fetal/neonatal adverse reactions premature closure of fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including celebrex, can cause premature closure of the fetal ductus arteriosus (see error! hyperlink reference not valid. ). oligohydramnios/neonatal renal impairment: if an nsaid is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. if celebrex treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue celebrex and follow up according to clinical practice (see error! hyperlink reference not valid. ). labor or delivery there are no studies on the effects of celebrex during labor or delivery. in animal studies, nsaids, including celecoxib, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data human data the available data do not establish the presence or absence of developmental toxicity related to the use of celebrex. premature closure of fetal ductus arteriosus: published literature reports that the use of nsaids at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment: published studies and postmarketing reports describe maternal nsaid use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. in many cases, but not all, the decrease in amniotic fluid was transient and reversible with cessation of the drug. there have been a limited number of case reports of maternal nsaid use and neonatal renal dysfunction without oligohydramnios, some of which were irreversible. some cases of neonatal renal dysfunction required treatment with invasive procedures, such as exchange transfusion or dialysis. methodological limitations of these postmarketing studies and reports include lack of a control group; limited information regarding dose, duration, and timing of drug exposure; and concomitant use of other medications. these limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal nsaid use. because the published safety data on neonatal outcomes involved mostly preterm infants, the generalizability of certain reported risks to the full-term infant exposed to nsaids through maternal use is uncertain. animal data celecoxib at oral doses ≥150 mg/kg/day (approximately 2 times the human exposure at 200 mg twice daily as measured by auc0–24 ), caused an increased incidence of ventricular septal defects, a rare event, and fetal alterations, such as ribs fused, sternebrae fused and sternebrae misshapen when rabbits were treated throughout organogenesis. a dose-dependent increase in diaphragmatic hernias was observed when rats were given celecoxib at oral doses ≥30 mg/kg/day (approximately 6 times human exposure based on the auc0–24 at 200 mg twice daily for ra) throughout organogenesis. in rats, exposure to celecoxib during early embryonic development resulted in pre-implantation and post-implantation losses at oral doses ≥50 mg/kg/day (approximately 6 times human exposure based on the auc0–24 at 200 mg twice daily for ra). celecoxib produced no evidence of delayed labor or parturition at oral doses up to 100 mg/kg in rats (approximately 7-fold human exposure as measured by the auc0–24 at 200 mg twice daily). the effects of celebrex on labor and delivery in pregnant women are unknown. risk summary limited data from 3 published reports that included a total of 12 breastfeeding women showed low levels of celebrex in breast milk. the calculated average daily infant dose was 10 to 40 mcg/kg/day, less than 1% of the weight-based therapeutic dose for a two-year old-child. a report of two breastfed infants 17 and 22 months of age did not show any adverse events. caution should be exercised when celebrex is administered to a nursing woman. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for celebrex and any potential adverse effects on the breastfed infant from the celebrex or from the underlying maternal condition. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including celebrex, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including celebrex, in women who have difficulties conceiving or who are undergoing investigation of infertility. celebrex is approved for relief of the signs and symptoms of juvenile rheumatoid arthritis in patients 2 years and older. safety and efficacy have not been studied beyond six months in children. the long-term cardiovascular toxicity in children exposed to celebrex has not been evaluated and it is unknown if long-term risks may be similar to that seen in adults exposed to celebrex or other cox-2 selective and non-selective nsaids [see boxed warning, warnings and precautions (5.5), and clinical studies (14.3) ]. the use of celecoxib in patients 2 years to 17 years of age with pauciarticular, polyarticular course jra or in patients with systemic onset jra was studied in a 12-week, double-blind, active controlled, pharmacokinetic, safety and efficacy study, with a 12-week open-label extension. celecoxib has not been studied in patients under the age of 2 years, in patients with body weight less than 10 kg (22 lbs), and in patients with active systemic features. patients with systemic onset jra (without active systemic features) appear to be at risk for the development of abnormal coagulation laboratory tests. in some patients with systemic onset jra, both celecoxib and naproxen were associated with mild prolongation of activated partial thromboplastin time (aptt) but not prothrombin time (pt). when nsaids including celecoxib are used in patients with systemic onset jra, monitor patients for signs and symptoms of abnormal clotting or bleeding, due to the risk of disseminated intravascular coagulation. patients with systemic onset jra should be monitored for the development of abnormal coagulation tests [see dosage and administration (2.4), warnings and precautions (5.15), adverse reactions (6.1), animal toxicology (13.2), clinical studies (14.3) ]. alternative therapies for treatment of jra should be considered in pediatric patients identified to be cyp2c9 poor metabolizers [see poor metabolizers of cyp2c9 substrates (8.8) ]. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [see warnings and precautions (5.1, 5.2, 5.3, 5.6, 5.14) ]. of the total number of patients who received celebrex in pre-approval clinical trials, more than 3,300 were 65–74 years of age, while approximately 1,300 additional patients were 75 years and over. no substantial differences in effectiveness were observed between these subjects and younger subjects. in clinical studies comparing renal function as measured by the gfr, bun and creatinine, and platelet function as measured by bleeding time and platelet aggregation, the results were not different between elderly and young volunteers. however, as with other nsaids, including those that selectively inhibit cox-2, there have been more spontaneous post-marketing reports of fatal gi events and acute renal failure in the elderly than in younger patients [see warnings and precautions (5.2, 5.6) ]. the daily recommended dose of celebrex capsules in patients with moderate hepatic impairment (child-pugh class b) should be reduced by 50%. the use of celebrex in patients with severe hepatic impairment is not recommended [see dosage and administration (2.7) and clinical pharmacology (12.3) ]. celebrex is not recommended in patients with severe renal insufficiency [see warnings and precautions (5.6) and clinical pharmacology (12.3) ]. in patients who are known or suspected to be poor cyp2c9 metabolizers (i.e., cyp2c9*3/*3), based on genotype or previous history/experience with other cyp2c9 substrates (such as warfarin, phenytoin) administer celebrex starting with half the lowest recommended dose. alternative management should be considered in jra patients identified to be cyp2c9 poor metabolizers [see dosage and administration (2.7) and clinical pharmacology (12.5) ].

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equate (wal-mart stores, inc.) - docusate sodium (unii: f05q2t2ja0) (docusate - unii:m7p27195ag) - docusate sodium 100 mg - stool softener laxative - relieves occasional constipation (irregularity) - generally produces bowel movement in 12 to 72 hours

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wal-mart stores, inc - camphor (synthetic) (unii: 5tjd82a1et) (camphor (synthetic) - unii:5tjd82a1et) - camphor (synthetic) 62 mg in 1 ml - cough suppressant temporarily relieves cough associated with a cold - a persistent or chronic cough such as occurs with smoking, emphsema or asthma - a cough that occurs with too much phlegm ( mucus) cough persists for more than 1 week, tends to recur or is accompanied by fever, rash or persisten headach.  a persistent cough may be a sign of a serious condition.

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wal-mart - salicylic acid (unii: o414pz4lpz) (salicylic acid - unii:o414pz4lpz) - salicylic acid 5 mg in 1 ml - acne medication for the treatment of acne

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wal-mart stores, inc. - povidone-iodine (unii: 85h0hzu99m) (iodine - unii:9679tc07x4) - first aid antiseptic first aid to help prevent the risk of infection in minor cuts, scrapes and burns - in the eyes or apply over large areas of the body - longer than 1 week unless directed by a doctor condition persists or gets worse    - condition persists or gets worse