Inpatient violence in a psychiatric hospital in the middle of the pandemic: clinical and community health aspects.

Healthcare workers are at a high risk of violence all over the world. The hostility toward nurses, physicians, and hospital staff has reached the point that it can be considered a public health problem. In this paper, we focus on the harassment, aggression, and violence that many healthcare workers have encountered while treating unstable psychiatric patients in the middle of the COVID-19 pandemic. We present a case with a history of violence toward mental health workers, review psychopathological and clinical aspects, and discuss how both the COVID-19 pandemic and current challenges in psychiatric hospital settings increase the frequency and severity of these attacks and how this affects the team on inpatient psychiatric units. We used the CARE guidelines to provide the most accurate and transparent information about the patient and relevant psychosocial aspects. We also pooled more than 20 unique sources to cover all aspects of violent behaviors in all psychiatric settings for all age groups. We concluded that a lack of nursing staff, the mental burden imposed by difficult patients, and poor communication between team members are some of the factors contributing to patient violence. An incomplete understanding of the problem creates barriers to change on both personal and systematic levels. Constant violence and abuse against healthcare workers cause stress, decreased productivity, and work dissatisfaction. To improve the safety of healthcare professionals, especially in inpatient psychiatric settings, several system-based changes should be implemented.

Malingering of Psychotic Symptoms in Psychiatric Settings: Theoretical Aspects and Clinical Considerations.

Malingering is the intentional production of false or grossly exaggerated physical or psychological symptoms motivated by external incentives. Although the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) does not list malingering in its diagnostic section and therefore does not identify it as a formal mental disorder, malingering and verified mental illness commonly coexist. Some subtypes of feigning behaviors, such as partial or pure malingering, dissimulation, and false imputation, can be suspected when patients have marked discrepancies between reported stressors and objective findings. The article discusses these three theoretical concepts with their possible clinical aspects, illustrating each phenomenon by clinical case with self-reported and/or observed psychotic symptoms. We summarized relevant findings and provided a review of clinical considerations that physicians can use to aid in the evaluation of psychotic symptoms in the context of those three concepts.

Distinct compartmentalization of NF-κB activity in crypt and crypt-denuded lamina propria precedes and accompanies hyperplasia and/or colitis following bacterial infection.

Citrobacter rodentium induces transmissible murine colonic hyperplasia (TMCH) and variable degrees of inflammation and necrosis depending upon the genetic background. Utilizing C. rodentium-induced TMCH in C3H/HeNHsd inbred mice, we observed significant crypt hyperplasia on days 3 and 7 preceding active colitis. NF-κB activity in the crypt-denuded lamina propria (CLP) increased within 24 h postinfection, followed by its activation in the crypts at day 3, which peaked by day 7. Increases in interleukin-α1 (IL-1α), IL-12(p40), and macrophage inflammatory protein 1α (MIP-1α) paralleled NF-κB activation, while increases in IL-1α/ß, IL-6/IL-12(p40)/granulocyte colony-stimulating factor (G-CSF)/keratinocyte-derived chemokine (KC)/monocyte chemotactic protein 1 (MCP-1), and MIP-1α followed NF-κB activation leading to significant recruitment of neutrophils to the colonic mucosa and increased colonic myeloperoxidase (MPO) activity. Phosphorylation of the crypt cellular and nuclear p65 subunit at serines 276 and 536 led to functional NF-κB activation that facilitated expression of its downstream target, CXCL-1/KC, during TMCH. Distinct compartmentalization of phosphorylated extracellular signal-regulated kinase 1 and 2 ([ERK1/2] Thr(180)/Tyr(182)) and p38 (Thr(202)/Tyr(204)) in the CLP preceded increases in the crypts. Inhibition of ERK1/2 and p38 suppressed NF-κB activity in both crypts and the CLP. Dietary administration of 6% pectin or 4% curcumin in C. rodentium-infected mice also inhibited NF-κB activity and blocked CD3, F4/80, IL-1α/ß, G-CSF/MCP-1/KC, and MPO activity in the CLP while not affecting NF-κB activity in the crypts. Thus, distinct compartmentalization of NF-κB activity in the crypts and the CLP regulates crypt hyperplasia and/or colitis, and dietary intervention may be a novel strategy to modulate NF-κB-dependent protective immunity to facilitate crypt regeneration following C. rodentium-induced pathogenesis.