University faculty on student motivation to use medical education apps and barriers to their usage.

OBJECTIVE: University teachers, who primarily provide guidance and advice to their students, can play a significant role in educational process transformation. As there is no particular e-learning framework, it is important to understand the factors and variables that may impact both its effective usage and further successful implementation. The current study aims to outline the influence of university faculty, and possible barriers preventing medical students from using apps for learning purposes. SUBJECTS AND METHODS: Α cross-sectional study was conducted with an online survey questionnaire. The population of the study included 1,458 students from all the seven Greek schools of medicine. RESULTS: University faculty (51.7%), followed by fellow students and friends (55.6%), constitute the second most common source of information on adopting apps for medical education. 45.8% of students rated their educational guidance as insufficient/inadequate, 33.0% as moderate, 18.6% as quite good, and only 2.7% as sufficient/complete. University professors have proposed certain apps to 25.5% of students. PubMed (41.7%), Medscape (20.9%), and Complete Anatomy (12.2%) were the leading suggestions. The main barriers to app usage were the lack of knowledge of apps' benefits (28.8%), insufficient updates of their content (21.9%), their cost-effectiveness (19.2%), and financial reasons (16.2%). Most students preferred using free apps (51.4%) and 76.7% preferred universities to cover apps' expenses. CONCLUSIONS: University faculty represent the main source of information regarding the adaptation of medical apps in the educational process. However, students need improved and enhanced guidance. The main barriers are ignorance about apps and financial reasons. The majority prefer free apps and universities to cover their cost.

Trace elements and the carotid plaque: the GOOD (Mg, Zn, Se), the UGLY (Fe, Cu), and the BAD (P, Ca)?

Multiple epidemiological studies have suggested that industrialization and progressive urbanization should be considered one of the main factors responsible for the rising of atherosclerosis in the developing world. In this scenario, the role of trace metals in the insurgence and progression of atherosclerosis has not been clarified yet. In this paper, the specific role of selected trace elements (magnesium, zinc, selenium, iron, copper, phosphorus, and calcium) is described by focusing on the atherosclerotic prevention and pathogenesis plaque. For each element, the following data are reported: daily intake, serum levels, intra/extracellular distribution, major roles in physiology, main effects of high and low levels, specific roles in atherosclerosis, possible interactions with other trace elements, and possible influences on plaque development. For each trace element, the correlations between its levels and clinical severity and outcome of COVID-19 are discussed. Moreover, the role of matrix metalloproteinases, a family of zinc-dependent endopeptidases, as a new medical therapeutical approach to atherosclerosis is discussed. Data suggest that trace element status may influence both atherosclerosis insurgence and plaque evolution toward a stable or an unstable status. However, significant variability in the action of these traces is evident: some - including magnesium, zinc, and selenium - may have a protective role, whereas others, including iron and copper, probably have a multi-faceted and more complex role in the pathogenesis of the atherosclerotic plaque. Finally, calcium and phosphorus are implicated in the calcification of atherosclerotic plaques and in the progression of the plaque toward rupture and severe clinical complications. In particular, the role of calcium is debated. Focusing on the COVID-19 pandemia, optimized magnesium and zinc levels are indicated as important protective tools against a severe clinical course of the disease, often related to the ability of SARS-CoV-2 to cause a systemic inflammatory response, able to transform a stable plaque into an unstable one, with severe clinical complications.

Síndrome de Kounis del tipo II inducido por amoxicilina-ácido clavulánico complicado con encefalopatía hipóxico-isquémica durante anestesia general / Amoxicillin-clavulanic acid-induced type II Kounis syndrome during general anaesthesia complicated with hypoxic-ischaemic encephalopathy

La anafilaxis es un síndrome multisistémico agudo grave que implica la liberación masiva del torrente sanguíneo de mastocitos y mediadores basófilos. Cuando las arterias coronarias son el objetivo principal, se puede sospechar el síndrome de Kounis o, más raramente, el llamado síndrome de Kounis cuando se trata de arterias cerebrales. Las lesiones isquémicas cerebrales pueden resultar de una presión arterial baja o de una acción mediadora proinflamatoria y/o vasoconstrictora directa en el sistema arterial cerebral. El diagnóstico es difícil en pacientes anestesiados. El tratamiento también es un reto, ya que la administración de adrenalina puede empeorar la isquemia. Presentamos un caso de síndrome de Kounis tipo II inducido por amoxicilina-ácido clavulánico bajo anestesia general, complicado con encefalopatía grave e irreversible de origen isquémico.(au)

Anaphylaxis is a severe acute multisystem syndrome involving massive mediator release from mast cells and basophils. Although the entire arterial system can be affected, when coronary arteries are the main targets, Kounis syndrome needs to be considered. Cerebral artery involvement has also been suggested in rarer MC-mediator release episodes; so-called ‘Kounis-like’ syndrome. Cerebral ischaemic lesions can then result from low blood pressure or direct proinflammatory and/or vasoconstrictive mediator action in the cerebral arterial system. Diagnosis can be difficult in anaesthetised patients, as low blood pressure can have multiple causes. Treatment is also challenging, as administering adrenaline can worsen ischaemia. We report the first case of amoxicillin-clavulanic acid-induced type II Kounis syndrome under general anaesthesia, complicated with severe, irreversible and subsequently fatal encephalopathy of ischaemic origin. This case can contribute to awareness of less common Kounis syndrome manifestations, including severe cerebral involvement, or other anaphylactic reactions with atypical presentations.(AU)

Amoxicillin-clavulanic acid-induced type II Kounis syndrome during general anaesthesia complicated with hypoxic-ischaemic encephalopathy. / Síndrome de Kounis del tipo II inducido por amoxicilina-ácido clavulánico complicado con encefalopatía hipóxico-isquémica durante anestesia general.

Anaphylaxis is a severe acute multisystem syndrome involving massive mediator release from mast cells and basophils. Although the entire arterial system can be affected, when coronary arteries are the main targets, Kounis syndrome needs to be considered. Cerebral artery involvement has also been suggested in rarer MC-mediator release episodes; so-called 'Kounis-like' syndrome. Cerebral ischaemic lesions can then result from low blood pressure or direct proinflammatory and/or vasoconstrictive mediator action in the cerebral arterial system. Diagnosis can be difficult in anaesthetised patients, as low blood pressure can have multiple causes. Treatment is also challenging, as administering adrenaline can worsen ischaemia. We report the first case of amoxicillin-clavulanic acid-induced type II Kounis syndrome under general anaesthesia, complicated with severe, irreversible and subsequently fatal encephalopathy of ischaemic origin. This case can contribute to awareness of less common Kounis syndrome manifestations, including severe cerebral involvement, or other anaphylactic reactions with atypical presentations.

WITHDRAWN: Amoxicillin-clavulanic acid-induced type II Kounis syndrome during general anaesthesia complicated with hypoxic-ischaemic encephalopathy.

The Publisher regrets that this article is an accidental duplication of an article that has already been published, https://doi.org/10.1016/j.redar.2019.06.002. The duplicate article has therefore been withdrawn. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal.

A joint allergist/cardiologist classification for thienopyridines hypersensitivity reactions based on their symptomatic patterns and its impact on the management strategies.

The role and importance of thienopyridines such as ticlopidine, clopidogrel, and prasugrel is well-established for several indications, ranging from prevention of acute coronary syndromes to percutaneous coronary interventions, where the dual antiplatelet therapy represents the gold standard to avoid denovo coronary stenosis. However, there is a significant cohort of patients with coronary artery disease who may manifest hypersensitivity reactions to thienopyridines. The examination of the various case reports from medical literature leads to identify mainly four clinical patterns of hypersensitivity to thienopyridines which involves more frequently cutaneous, hematologic, and articular tissues, therefore the kind and predominance of clinical symptoms may determine a different clinical approach to overcome or neutralize thienopyridines hypersensitivity.

The more allergens an atopic patient is exposed to, the easier and quicker anaphylactic shock and Kounis syndrome appear: Clinical and therapeutic paradoxes.

Kounis syndrome is a condition that combines allergic, hypersensitivity, anaphylactic or anaphylactoid reactions with acute coronary syndromes including vasospastic angina, acute myocardial infarction and stent thrombosis. This syndrome is a ubiquitous disease affecting patients of any age, involving numerous and continuously increasing causes, with broadening clinical manifestations and covering a wide spectrum of mast cell activation disorders. Drugs, environmental exposures and various conditions are the main offenders. Clinical and therapeutic paradoxes concerning Kounis syndrome therapy, pathophysiology, clinical course and causality have been encountered during its clinical course. Drugs that counteract allergy, such as H2-antihistamines, can induce allergy and Kounis syndrome. The more drugs an atopic patient is exposed to, the easier and quicker anaphylaxis and Kounis syndrome can occur. Every anesthetized patient is under the risk of multiple drugs and substances that can induce anaphylactic reaction and Kounis syndrome. The heart and the coronary arteries seem to be the primary target in severe anaphylaxis manifesting as Kounis syndrome. Commercially available adrenaline saves lives in anaphylaxis but it contains as preservative sodium metabisulfite and should be avoided in the sulfite allergic patients. Thus, careful patient past history and consideration for drug side effects and allergy should be taken into account before use. The decision to prescribe a drug where there is a history of previous adverse reactions requires careful assessment of the risks and potential benefits.