Nurse Practitioner Certification Examination Development: From Reflecting Clinical Practice to Ensuring Lifelong Learning.

OBJECTIVE: Certifications in psychiatric-mental health nursing promote safe practice by psychiatric-mental health nurse practitioners (PMHNPs) and nurses (PMHNs) and help protect the public from harm. This protection begins with the development of an examination that meets rigorous national education, practice, and accreditation standards and reflects PMHNPs' or PMHNs' clinical practice. Achievement and maintenance of a certification is a journey that involves a commitment to lifelong learning and the improvement of the field of psychiatric-mental health nursing through involvement in the examination process. METHODS: This discussion paper outlines the role nurses can play in the development of certification examinations. It describes the process of developing an effective certification examination, including the role of standards, accrediting bodies, and content experts; determining necessary tasks, knowledge, and skills; surveying practitioners to validate information; writing test questions; and ongoing analysis of examination content. The Psychiatric-Mental Health Nurse Practitioner (across the lifespan) Certification (PMHNP-BC) is presented as an example of the process. RESULTS: This discussion paper raises awareness of how certification exams are developed, PMHNPs participate in certification development, and volunteering promotes career development. CONCLUSION: The PMHNP-BC examination is based on education, practice, and certification accreditation standards and reflects current clinical practice. PMHNPs can (a) point to the rigor of certification as an indication of the quality of care they deliver, (b) volunteer to participate in the examination process to ensure examination rigor, and (c) advance their careers through the development and application of a valuable skill set.

Health outcomes and healthcare utilization of Native Hawaiians and other Pacific Islanders living with HIV in Hawai'i: A mixed-methods study.

OBJECTIVES: Past research shows mixed outcomes in terms of HIV-related disparities among Native Hawaiians and Pacific Islanders (NHOPI). This study investigates HIV-related disparities among NHOPI living with HIV in Hawai'i. DESIGN: An explanatory sequential design was utilized. The quantitative portion analyzed survey data from a statewide Ryan White Needs Assessment (N = 398) to examine the differences in viral suppression and satisfaction with care between NHOPI and other ethnic groups. Utilizing the behavioral model for vulnerable populations (BMVP), semi-structured interviews (N = 16) were conducted next to explain what factors play a role in satisfaction with care and viral suppression when it comes to NHOPI living with HIV in Hawai'i. RESULTS: Among the 398 participants 13% were NHOPI. NHOPI were more likely to have a viral load of ≥10,000 copies/mL compared to those who didn't identify as NHOPI. However, there were no significant differences for other viral load levels (20-199 or 200-9999), and only 20 participants (5.2%) had a viral load of 10,000 copies/mL or more. No significant ethnic differences were found in satisfaction with medical care. In the qualitative phase, factors from all domains of the BMVP were represented within the four themes identified: (1) Care coordination is essential- with AIDs service organizations taking the lead; (2) HIV care, as well as overall health, is defined by the effectiveness of medication; (3) Initial diagnosis is a critical moment for intervention; and (4) Aspects of culture are intangible. CONCLUSION: Among NHOPI in Hawai'i who are engaged in case management, there appears to be no substantial disparities in either viral load or satisfaction with care compared to other ethnic groups. Despite this, qualitative findings provide insights on how ethnicity and culture may still be playing a role. Addressing all domains of the BMVP is crucial to addressing this.

Matchmaking facilitates the diagnosis of an autosomal-recessive mitochondrial disease caused by biallelic mutation of the tRNA isopentenyltransferase (TRIT1) gene.

Deleterious variants in the same gene present in two or more families with overlapping clinical features provide convincing evidence of a disease-gene association; this can be a challenge in the study of ultrarare diseases. To facilitate the identification of additional families, several groups have created "matching" platforms. We describe four individuals from three unrelated families "matched" by GeneMatcher and MatchMakerExchange. Individuals had microcephaly, developmental delay, epilepsy, and recessive mutations in TRIT1. A single homozygous mutation in TRIT1 associated with similar features had previously been reported in one family. The identification of these individuals provides additional evidence to support TRIT1 as the disease-causing gene and interprets the variants as "pathogenic." TRIT1 functions to modify mitochondrial tRNAs and is necessary for protein translation. We show that dysfunctional TRIT1 results in decreased levels of select mitochondrial proteins. Our findings confirm the TRIT1 disease association and advance the phenotypic and molecular understanding of this disorder.

Ketogenic diet efficacy in the treatment of intractable epileptic spasms.

OBJECTIVE: To determine the efficacy of the ketogenic diet in controlling epileptic spasms after failing traditional antiepileptic medication therapy. METHODS: This is a prospective, case-based study of all infants with epileptic spasms who were referred for treatment with the ketogenic diet at our hospital between 2009 and 2012. All subjects continued to have epileptic spasms with evidence of hypsarrhythmia or severe epileptic encephalopathy on electroencephalography despite appropriate medication treatments. The diet efficacy was assessed through clinic visits, phone communications, and electroencephalography. Quality of life improvement was charted based on the caregiver's perspective. RESULTS: Twenty infants (15 males) were included in the study. The mean age at seizure onset was 4.5 months. Age at ketogenic diet initiation was 0.3 to 2.9 years (mean 1.20, standard deviation 0.78). Fifteen patients had epileptic spasms of unknown etiology; three had perinatal hypoxic ischemic encephalopathy, one had lissencephaly, and one had STXBP1 mutation. Fifteen infants failed to respond to adrenocorticotropin hormone and/or vigabatrin before going on the ketogenic diet. Three months after starting the diet, >50% seizure reduction was achieved in 70% of patients (95% CI 48-86). These results were maintained at 6- and 12-month intervals. All eight of the patients followed for 24 months had >50% seizure reduction (95% CI 63-100). At least 90% seizure reduction was reported in 20% of patients at 3 months (95% CI 7-42), 22% (95% CI 8-46) at 6 months, and 35% (95% CI 17-59) at 12 months. The majority of patients (63%) achieved improvement of their spasms within 1 month after starting the diet. Sixty percent of patients had electroencephalographic improvement. All caregivers reported improvement of the quality of life at the 3-month visit (95% confidence interval 81-100). This ratio was 94% at 6 months (95% CI 72-99) and 82% at 12 months (95% CI 58-95). CONCLUSION: The ketogenic diet is a safe and potentially effective method of treatment for patients with epileptic spasms, especially those who do not respond to customary medication therapies.