Achieving Royal Pharmaceutical Society competencies: a frailty nurse's perspective

2019 ◽  
Vol 1 (1) ◽  
pp. 44-48
Author(s):  
Joanna Banks
Keyword(s):  
At Risk ◽  
Adverse Outcomes ◽  
Competency Framework ◽  
Ageing Process ◽  
Frail Patients ◽  
Pharmaceutical Society ◽  
Medication Reviews ◽  
Regular Medication ◽  
Royal Pharmaceutical Society

Frailty is related to the ageing process and describes how a person's inbuilt reserve struggles to withstand major changes in health, such as infection, a change to medication or a new environment. The British Geriatric Society (2014) approximate that around 10% of people over the age of 65 years have frailty rising to between a quarter to a half of those aged over 85 years. Patients who are deemed frail are often at risk of adverse outcomes; therefore, it is important to seek out these individuals and care for them appropriately. This includes carrying out regular medication reviews and deprescribing where necessary. This article will discuss prescribing for frail patients using the Royal Pharmaceutical Society's Competency Framework for all Prescribers.

Developing a competency framework for designated prescribing practitioners

2020 ◽  
Vol 2 (5) ◽  
pp. 252-256
Author(s):  
Adele Mott
Keyword(s):  
Local Variation ◽  
Competency Framework ◽  
Regulatory Changes ◽  
Pharmaceutical Society ◽  
User Groups ◽  
Royal Pharmaceutical Society

In 2019, the Royal Pharmaceutical Society published a Competency Framework for Designated Prescribing Practitioners to support the implementation of regulatory changes and underpin quality in training of non-medical prescribers during the period of learning in practice. This article takes a look at the need for, development, scope and content of the framework, and considers its implementation in practice. The framework has been developed to support quality in training during the period of learning in practice. It is designed for use by a broad range of user groups across different professions and settings, as such, some contextualisation of the content is needed and there will be local variation in how it is used in practice.

scholarly journals Chitinase 3 like 1 is a regulator of smooth muscle cell physiology and atherosclerotic lesion stability

2021 ◽  
Author(s):  
Pavlos Tsantilas ◽  
Shen Lao ◽  
Zhiyuan Wu ◽  
Anne Eberhard ◽  
Greg Winski ◽  
...  
Keyword(s):  
At Risk ◽  
Smooth Muscle ◽  
Carotid Artery ◽  
Atherosclerotic Lesion ◽  
Adverse Outcomes ◽  
Plaque Burden ◽  
Cell Physiology ◽  
Mechanistic Studies ◽  
Plaque Vulnerability ◽  
Fibrous Cap

Abstract Aims  Atherosclerotic cerebrovascular disease underlies the majority of ischaemic strokes and is a major cause of death and disability. While plaque burden is a predictor of adverse outcomes, plaque vulnerability is increasingly recognized as a driver of lesion rupture and risk for clinical events. Defining the molecular regulators of carotid instability could inform the development of new biomarkers and/or translational targets for at-risk individuals. Methods and results  Using two independent human endarterectomy biobanks, we found that the understudied glycoprotein, chitinase 3 like 1 (CHI3L1), is up-regulated in patients with carotid disease compared to healthy controls. Further, CHI3L1 levels were found to stratify individuals based on symptomatology and histopathological evidence of an unstable fibrous cap. Gain- and loss-of-function studies in cultured human carotid artery smooth muscle cells (SMCs) showed that CHI3L1 prevents a number of maladaptive changes in that cell type, including phenotype switching towards a synthetic and hyperproliferative state. Using two murine models of carotid remodelling and lesion vulnerability, we found that knockdown of Chil1 resulted in larger neointimal lesions comprised by de-differentiated SMCs that failed to invest within and stabilize the fibrous cap. Exploratory mechanistic studies identified alterations in potential downstream regulatory genes, including large tumour suppressor kinase 2 (LATS2), which mediates macrophage marker and inflammatory cytokine expression on SMCs, and may explain how CHI3L1 modulates cellular plasticity. Conclusion  CHI3L1 is up-regulated in humans with carotid artery disease and appears to be a strong mediator of plaque vulnerability. Mechanistic studies suggest this change may be a context-dependent adaptive response meant to maintain vascular SMCs in a differentiated state and to prevent rupture of the fibrous cap. Part of this effect may be mediated through downstream suppression of LATS2. Future studies should determine how these changes occur at the molecular level, and whether this gene can be targeted as a novel translational therapy for subjects at risk of stroke.

Maternal Thinness and Obesity and Customized Fetal Weight Charts

2021 ◽  
pp. 1-9
Author(s):  
Nieves L. González González ◽  
Enrique González Dávila ◽  
Agustina González Martín ◽  
Erika Padrón ◽  
José Ángel García Hernández
Keyword(s):  
At Risk ◽  
Gestational Age ◽  
Neonatal Intensive Care ◽  
Perinatal Outcomes ◽  
Adverse Outcomes ◽  
Analysis Of Covariance ◽  
Large For Gestational Age ◽  
Perinatal Morbidity ◽  
Accurate Identification ◽  
Cephalopelvic Disproportion

<b><i>Objective:</i></b> The aim of the study was to determine if customized fetal growth charts developed excluding obese and underweight mothers (CC<sub>(18.5–25)</sub>) are better than customized curves (CC) at identifying pregnancies at risk of perinatal morbidity. <b><i>Material and Methods:</i></b> Data from 20,331 infants were used to construct CC and from 11,604 for CC<sub>(18.5–25)</sub>, after excluding the cases with abnormal maternal BMI. The 2 models were applied to 27,507 newborns and the perinatal outcomes were compared between large for gestational age (LGA) or small for gestational age (SGA) according to each model. Logistic regression was used to calculate the OR of outcomes by the group, with gestational age (GA) as covariable. The confidence intervals of pH were calculated by analysis of covariance. <b><i>Results:</i></b> The rate of cesarean and cephalopelvic disproportion (CPD) were higher in LGA<sub>only by CC</sub><sub><sub>(18.5−25)</sub></sub> than in LGA<sub>only by CC</sub>. In SGA<sub>only by CC</sub><sub><sub>(18.5−25)</sub></sub>, neonatal intensive care unit (NICU) and perinatal mortality rates were higher than in SGA<sub>only by CC</sub>. Adverse outcomes rate was higher in LGA<sub>only by CC</sub><sub><sub>(18.5−25)</sub></sub> than in LGA<sub>only by CC</sub> (21.6%; OR = 1.61, [1.34–193]) vs. (13.5%; OR = 0.84, [0.66–1.07]), and in SGA <sub>only by CC</sub><sub><sub>(18.5−25)</sub></sub> than in SGA<sub>only by CC</sub> (9.6%; OR = 1.62, [1.25–2.10] vs. 6.3%; OR = 1.18, [0.85–1.66]). <b><i>Conclusion:</i></b> The use of CC<sub>(18.5–25)</sub> allows a more accurate identification of LGA and SGA infants at risk of perinatal morbidity than conventional CC. This benefit increase and decrease, respectively, with GA.

scholarly journals Small Dense Low-Density Lipoprotein: Biomarker or Potential Drug Target?

2019 ◽  
Vol 55 (02) ◽  
pp. 092-097
Author(s):  
Basabdatta Samanta
Keyword(s):  
At Risk ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Adverse Outcomes ◽  
Ischemic Heart ◽  
Low Density ◽  
Treatment And Prevention ◽  
Artery Disease

AbstractIschemic heart disease is currently an epidemic affecting individuals worldwide. Increased incidence along with earlier onset of disease has led to the constant search for biomarkers that will help in earlier identification and treatment of at risk individuals. Small dense low-density lipoprotein (sdLDL) is the atherogenic subtype of low-density lipoprotein (LDL). It is smaller in size and higher in density in comparison to other LDL subtypes. Higher levels of sdLDL have beenfound to be associated with increased incidence of ischemic heart disease and adverse outcomes. Properties including decreased resistance to oxidative stress and prolonged residence time in the circulation account for its increased atherogenic potential. Hence intervention approaches targeting sdLDL directly in at risk individuals may be beneficial.Genetic, lifestyle, and environmental factors affect sdLDL levels.But the main determining factor is the level of triglycerides (TGs). Higher TG levels are associated with higher levels of very low density lipoprotein (VLDL) 1 and sdLDL. Various drugs have been used for targeting sdLDL with varying outcomes; drugs tried out include statins, fibrates, niacin, cholesterol ester transfer protein inhibitors and sodium-glucose co-transporter-2 inhibitors. Future prospects include modification of enzymes involved in fatty acid and TG synthesis, for example, lipoprotein lipase and acyl CoA carboxylase. However, further research is still necessary to draw clear guidelines for sdLDL reduction therapy in coronary artery disease treatment and prevention.

scholarly journals Sepsis in the era of data-driven medicine: personalizing risks, diagnoses, treatments and prognoses

2019 ◽  
Vol 21 (4) ◽  
pp. 1182-1195
Author(s):  
Andrew C Liu ◽  
Krishna Patel ◽  
Ramya Dhatri Vunikili ◽  
Kipp W Johnson ◽  
Fahad Abdu ◽  
...  
Keyword(s):  
At Risk ◽  
Data Science ◽  
Drug Repositioning ◽  
Healthcare Delivery ◽  
Heterogeneous Data ◽  
Machine Intelligence ◽  
Adverse Outcomes ◽  
Data Driven ◽  
Biomedical Data ◽  
Prolonged Stay

Abstract Sepsis is a series of clinical syndromes caused by the immunological response to infection. The clinical evidence for sepsis could typically attribute to bacterial infection or bacterial endotoxins, but infections due to viruses, fungi or parasites could also lead to sepsis. Regardless of the etiology, rapid clinical deterioration, prolonged stay in intensive care units and high risk for mortality correlate with the incidence of sepsis. Despite its prevalence and morbidity, improvement in sepsis outcomes has remained limited. In this comprehensive review, we summarize the current landscape of risk estimation, diagnosis, treatment and prognosis strategies in the setting of sepsis and discuss future challenges. We argue that the advent of modern technologies such as in-depth molecular profiling, biomedical big data and machine intelligence methods will augment the treatment and prevention of sepsis. The volume, variety, veracity and velocity of heterogeneous data generated as part of healthcare delivery and recent advances in biotechnology-driven therapeutics and companion diagnostics may provide a new wave of approaches to identify the most at-risk sepsis patients and reduce the symptom burden in patients within shorter turnaround times. Developing novel therapies by leveraging modern drug discovery strategies including computational drug repositioning, cell and gene-therapy, clustered regularly interspaced short palindromic repeats -based genetic editing systems, immunotherapy, microbiome restoration, nanomaterial-based therapy and phage therapy may help to develop treatments to target sepsis. We also provide empirical evidence for potential new sepsis targets including FER and STARD3NL. Implementing data-driven methods that use real-time collection and analysis of clinical variables to trace, track and treat sepsis-related adverse outcomes will be key. Understanding the root and route of sepsis and its comorbid conditions that complicate treatment outcomes and lead to organ dysfunction may help to facilitate identification of most at-risk patients and prevent further deterioration. To conclude, leveraging the advances in precision medicine, biomedical data science and translational bioinformatics approaches may help to develop better strategies to diagnose and treat sepsis in the next decade.

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