Increasing Hospital Pharmacist Clinical Competence in Intensive Pharmacotherapeutics Using a Novel Pharmacist Clinical Educational Program

Background:

Intensive pharmacotherapeutics (IP) is the application of multiple evidence-based practices applied at a patient-specific level, creating the overall best treatment plan in medically complex patients. To practice at this level, a high level of clinical knowledge and competency is paramount.

Objective:

The goal of the pharmacist clinical educational program was to develop an engaging, challenging, and interactive program, which was concise but intense, to improve pharmacists’ clinical knowledge and critical thinking skills.

Methods:

A 12-week educational series was developed and successfully implemented. The primary outcome was a comparison of the proportion of accepted clinical interventions per total number of medication orders reviewed by hospital pharmacists during and after the pharmacist clinical educational program to a 3-month baseline. The secondary outcome was to anonymously gauge participant satisfaction with the program.

Results:

The proportion of accepted clinical interventions increased from 6.4% (at baseline) to 9.1% and 8.7% in the 3 months during and 3 months immediately after the educational program, respectively (P < .01). The overall acceptance rate for clinical interventions remained >90% for all periods. Approximately 94% of respondents (n = 16) indicated that the program met their educational needs.

Conclusions:

The development of a clinical educational program to engage, challenge, and incentivize pharmacists is an essential tool to elevate the practice of IP. By maximizing existing resources, programming can be provided in an efficient and cost-effective manner. As health systems continue to merge on a national level, the methods described here demonstrate a means to provide critical education for both clinical and organizational competency.     

Health care seeking among detained undocumented migrants: a cross-sectional study

Background  

As in many European countries, access to care is decreased for undocumented migrants in the Netherlands due to legislation. Studies on the health of undocumented migrants in Europe are scarce and focus on care-seeking migrants. Not much is known on those who do not seek care.     

"Stem cell" origin of the hematopoietic defect in dyskeratosis congenita

We have used the long-term bone marrow culture (LTBMC) system to analyze hematopoiesis in three patients with dyskeratosis congenita (DC), two of whom had aplastic anemia, and the third had a normal blood count (apart from mild macrocytosis) and normal BM cellularity. Hematopoiesis was severely defective in all three patients, as measured by a low incidence of colony-forming cells and a low level of hematopoiesis in LTBMC. The function of the marrow stroma was normal in its ability to support the growth of hematopoietic progenitors from normal marrows seeded onto them in all three cases, but the generation of hematopoietic progenitors from patients marrow cells inoculated onto normal stromas was reduced, thus suggesting the defect to be of stem cell origin. The parents and unaffected brother of one of the families have also been studied in LTBMC and all showed normal hematopoietic and stromal cell function. From this study we speculate that there are some similarities between DC and the defect in the W/Wv mouse.     

Chronic hemolytic anemia due to a monoclonal IgG cold agglutinin with anti-Pr specificity

Immunologic studies performed in a case of autoimmune chronic hemolytic anemia with low titer cold agglutinins (1/16) demonstrated that the cold agglutinins corresponded to monoclonal IgG with anti-Pr specificity. This antibody had a large thermal amplitude, being active at 37 degrees C. These unusual characteristics may define a distinct subset of chronic cold agglutinin disease.     

The use of 7-amino actinomycin D in identifying apoptosis: simplicity of use and broad spectrum of application compared with other techniques

The detection and quantitation of apoptotic cells is becoming increasingly important in the investigation of the role of apoptosis in cellular proliferation and differentiation. The pathogenesis of hematologic disorders such as aplastic anemia and the development of neoplasia are believed to involve dysregulation of apoptosis. To quantitate accurately the proportion of apoptosis cells within different cell types of a heterogeneous cell population such as blood or bone marrow, a method is required that combines the analysis of large numbers of cells with concurrent immunophenotyping of cell surface antigens. In this study, we have evaluated such a method using the fluorescent DNA binding agent, 7-amino actinomycin D (7AAD), to stain three diverse human cell lines, induced to undergo apoptosis by three different stimuli. Flow cytometric analysis defines three populations on the basis of 7AAD fluorescence and forward light scatter. We have shown by cell sorting and subsequent morphological assessment and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling that the populations defined by 7AAD represent live, apoptotic, and late-apoptotic/dead cells. This method is quick, simple, reproducible, and cheap and will be a valuable tool in the investigation of the role of apoptosis in normal physiology and in disease states.     

Normal synthesis and expression of endothelial IIb/IIIa in Glanzmann's thrombasthenia

Glanzmann's thrombasthenia is a bleeding disorder, inherited in an autosomal recessive way and characterized by an absence or deficiency of the platelet glycoprotein (GP) IIb/IIIa complex. Recently, we and others demonstrated that cultured human umbilical vein endothelial cells synthesized a membrane protein complex similar to the platelet GP IIb/IIIa complex. In this article, we demonstrate that endothelial cells isolated from the umbilical vein of a newborn with Glanzmann's thrombasthenia, as compared with normal endothelial cells, show no difference in their ability to synthesize and express this GP IIb/IIIa complex. Our results indicate that Glanzmann's thrombasthenia is not accompanied by an "endotheliopathy."     

Immunologic injury to vascular endothelial cells: effects on release of prostacyclin

Prostacyclin is released from cultured and ex vivo bovine vascular endothelium following sublethal immunologic injury by a heterologous antibody to endothelial cells developed in rabbits. This release was dependent on calcium and complement and was not enhanced by the presence of platelets. Prostacyclin release was diminished 1-2 hr after the injury, but recovered fully following reculture of the endothelial cells for 72 hr.     

Enhancement of chemotactic factor-stimulated neutrophil oxidative metabolism by leukotriene B4

Leukotriene B4 (LTB4) is a potent primary stimulator of neutrophil chemotaxis, aggregation, and degranulation and induces superoxide production at higher concentrations. In order to determine whether LTB4 modulates neutrophil responses to oxidative stimuli, human neutrophils (PMNs) were incubated with LTB4 prior to stimulation with f-Met-Leu-Phe (fMLP, 10(-7) mol/L), opsonized zymosan (OZ, 250 micrograms/mL), or phorbol myristate acetate (PMA, 32 nmol/L). Superoxide (O2-) production by stimulated PMNs was assessed by the superoxide dismutase-inhibitable reduction of cytochrome c. LTB4 alone did not stimulate O2- production in concentrations below 10(-7) mol/L and had no effect on the O2- assay. In the concentration range of 10(-12) to 10(-8) mol/L, LTB4 did not alter O2- release induced by OZ or PMA. In contrast, LTB4-treated cells demonstrated enhanced O2- production following exposure to fMLP, and in the presence of 10 nmol/LLTB4, generated 180% +/- 41% of O-2 quantities produced by control cells (n = 23). Enhancement was LTB4 dose-dependent, was maximal in the range of 1 to 10 nmol/L LTB4, was not reversed by removal of the lipid from the medium prior to fMLP stimulation, and was not dependent on the presence of Ca++ or Mg++ in the suspending medium. Chemiluminescence of fMLP-stimulated neutrophils was increased to 323% of controls in neutrophils preincubated with 10 nmol/L LTB4. Unlike augmentation of oxidative responses to fMLP seen with other degranulating stimuli, enhancement by LTB4 was not correlated with an increase in 3H-fMLP receptor binding. These results indicate that, in addition to its primary effects on neutrophil function, LTB4 modulates PMN oxidative responses to the chemotactic peptide and, thus, may amplify the release of oxygen metabolites at inflammatory foci.