Emergency contraception: are pediatric residents counseling and prescribing to teens?

STUDY OBJECTIVES: (1) To assess pediatric residents' attitudes and practices related to counseling about and prescribing emergency contraceptive pills (ECPs) for teens. (2) To determine whether attitudes, counseling, and prescribing practices vary among different levels of residency training. DESIGN: Questionnaire. SETTING: Two large inner-city academic medical centers in New York City. PARTICIPANTS: Pediatric residents (PGY 1-3). MAIN OUTCOME MEASURES: Attitudes, counseling and prescribing patterns of ECPs by the pediatric residents RESULTS: 101/120 residents participated in the survey; 35% PGY1, 38% PGY2, 28% PGY3. Less than a third (26%) reported counseling teens about the availability of ECPs during routine non-acute care visits and just over half (56%) provided ECP counseling during visits for contraception. Only 6% of pediatric residents reported that they prescribed ECPs often, while 42% never prescribed ECPs. The majority of the residents did not think that prescribing ECPs would encourage teens to practice unsafe sex or would discourage compliance with other contraceptive methods (70% and 68%, respectively). However, the majority (67%) also reported that they did not think that ECPs should be available over the counter, without prescription. Further analysis by year of training showed that more junior and senior residents than interns counseled adolescents about ECPs at both routine health care maintenance visits and at visits for contraception (32% vs 15%; 62% vs 42%, respectively), would provide adolescent girls with ECPs to have on hand prior to an episode of unprotected sex (52% vs 31%), and thought that ECPs should be available over the counter (39% vs 20%), P < 0.05. CONCLUSIONS: Pediatric residents are missing opportunities to prevent unintended teenage pregnancy but they become more likely to counsel about and prescribe ECPs as they progress through residency training.

Myocardial cytochrome oxidase activity is decreased following carbon monoxide exposure.

Carbon monoxide (CO) inhalation often leads to cardiac dysfunction, dysrhythmias, ischemia, infarction, and death. However, the underlying mechanism of CO toxicity is poorly understood. We hypothesize that inhaled CO interrupts myocardial oxidative phosphorylation by decreasing the activity of myocardial cytochrome oxidase (CcOX), the terminal oxidase of the electron transport chain. Male C57Bl6 mice were exposed to either 1000 ppm (0.1%) CO or air for 3 h. Cardiac ventricles were harvested and mitochondria were isolated. CcOX kinetics and heme aa(3) content were measured. V(max), K(m), and turnover number were determined. Levels of CcOX subunit I message and protein were evaluated. Carboxyhemoglobin (COHb) levels were measured and tissue hypoxia was assessed with immunohistochemistry for pimonidazole hydrochloride. CO significantly decreased myocardial CcOX activity and V(max) without altering K(m). Heme aa(3) content and CcOX I protein levels significantly decreased following CO exposure while enzyme turnover number and CcOX I mRNA levels remained unchanged. CO exposure increased COHb levels without evidence of tissue hypoxia as compared to sham and hypoxic controls. Decreased CcOX activity following CO inhalation was likely due to decreased heme aa(3) and CcOX subunit I content. Importantly, myocardial CcOX impairment could underlie CO induced cardiac dysfunction.