Appendiceal adenocarcinoma presenting as left-sided large bowel obstruction,a case report and literature review

Background

appendiceal tumours are rare, they may be encountered unexpectedly in any acute or elective abdominal operation, many of these tumours are not appreciated intraoperatively and are diagnosed only during formal histopathological analysis of an appendicectomy specimen. Herein we present a case of appendiceal adenocarcinoma presenting as left-sided large bowel obstruction, we also review the literature of unusual presentations of appendiceal tumours.

Case Presentation

we report a case of left sided large bowel obstruction found to be secondary to an appendiceal adenocarcinoma. The patient presented with abdominal pain, distension and constipation, CT scan showed large bowel obstruction thought to be due to a sigmoid tumour, on laparotomy the appendix was also noted to be abnormal. A low Hartman's was performed with en-bloc total hysterectomy and bilateral salpigo-oophorectomy. A separate ileocaecal resection with end ileostomy was also performed, pathology specimens showed that the primary neoplasm was the appendix with metastasis to the distal sigmoid.

Conclusion

appendiceal tumours are rare, they usually present as acute appendicitis, other presentations are far less common.

     

Ultrastructural characterization of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-induced cell death in embryonic dopaminergic neurons

Developing neuronal populations undergo significant attrition by natural cell death. Dopaminergic neurons in the substantia nigra pars compacta undergo apoptosis during synaptogenesis. Following this time window, destruction of the anatomic target of dopaminergic neurons results in dopaminergic cell death but the morphology is no longer apoptotic. We describe ultrastructural changes that appear unique to dying embryonic dopaminergic neurons. In primary cultures of mesencephalon, death of dopaminergic neurons is triggered by activation of glutamate receptors sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and differs ultrastructurally from both neuronal apoptosis or typical excitotoxicity. AMPA causes morphological changes selectively in dopaminergic neurons, without affecting other neurons in the same culture dishes. Two hours after the onset of treatment swelling of Golgi complexes is apparent. At 3 h, dopaminergic neurons display loss of membrane asymmetry (coinciding with commitment to die), as well as nuclear membrane invagination, irregular aggregation of chromatin, and mitochondrial swelling. Nuclear changes continue to worsen until loss of cytoplasmic structures and cell death begins to occur after 12 h. These changes are different from those described in neurons undergoing either apoptosis or excitotoxic death, but are similar to ultrastructural changes observed in spontaneous death of dopaminergic neurons in the natural mutant weaver mouse.     

Glutamatergic neurotransmission in alcoholism

Substance abuse and dependence is the most common psychiatric problem. Alcohol is the most commonly abused substance and most people who abuse other substance(s) abuse alcohol at the same time. Accumulating evidence suggests that neurophysiological and pathological effects of ethanol are mediated to a considerable extent via the glutamatergic system. Ethanol disrupts glutamatergic neurotransmission by inhibiting the response of the N-methyl-D-aspartate (NMDA) receptor and by promoting neuronal toxicity through upregulation of the NMDA receptor density. Therefore, short-term/acute ethanol treatment results in a blockade of NMDA receptor-mediated neurotransmission and apoptotic cell death by inhibiting the trophic effect mediated by the NMDA receptor whereas chronic ethanol treatment and withdrawal results in an enhanced toxic response toward glutamate. The neurobiology of human alcoholism such as ethanol intoxication, dependence, withdrawal seizures, delirium tremens, Wernicke-Korsakoff syndrome, and fetal alcohol syndrome can be better understood as a spectrum of consequences of ethanol's effect on the NMDA glutamatergic system.