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Cocaine pathophysiology

Kosten TR Pathophysiology and treatment of cocaine dependence, in Neuropsychopharmacology The Fifth Generation of Progress. Edited by Davis KL, Charney D, Coyle JT, et al. Baltimore, MD, Lippincott Williams Wilkins, 2002, pp 1461-1473... [Pg.205]

Midline nasal and hard palate destruction have been reported in two chronic users of intranasal cocaine (118). The pathophysiology of these lesions is multifactorial, including ischemia secondary to vasoconstriction, chemical irritation from adulterants, impaired mucociliary transport, reduced immunity, and infection secondary to trauma. [Pg.499]

After an extensive literature search, the authors reported that the main pathophysiological mechanism underlying cocaine associated rhabdomyolysis is unknown. They suggested that cocaine blocks the reuptake of noradrenaline and dopamine, resulting in increased sympathetic activity. This, coupled with potent vasoconstriction by the cocaine metabolite benzoylecgo-nine, can lead to skeletal muscle ischemia and injury and result in rhabdomyolysis. [Pg.509]

Brownlow HA and Pappachan J (2002) Pathophysiology of cocaine abuse. European Journal of Anaesthesiology 19(6) 395-414. [Pg.634]

Cardiovascular toxicity due to cocaine abuse forms a spectrum of adverse medical conditions. The pathophysiology of cardiovascular events has been reviewed [21 ]. Ischemia and vasospasm are adrenergically mediated and there is a prothrombotic effect due to increased platelet aggregability. In the setting of hjrpoxia, intracoronary thrombosis can occur. [Pg.59]


See other pages where Cocaine pathophysiology is mentioned: [Pg.891]    [Pg.550]    [Pg.948]    [Pg.138]    [Pg.41]    [Pg.506]    [Pg.512]    [Pg.891]    [Pg.187]    [Pg.849]    [Pg.274]    [Pg.50]   
See also in sourсe #XX -- [ Pg.527 ]




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