RESUMEN
Recently termed pancreoprivic diabetes, type 3c diabetes refers to high blood sugar values secondary to disease of the exocrine pancreas. The disease is most commonly misdiagnosed as type 2 diabetes mellitus (DM) and is overlooked by physicians and the general public. Chronic pancreatitis (CP) accounts for most cases of type 3c diabetes. Diabetic ketoacidosis (DKA) is a rare occurrence in type 3c diabetes as both alpha and beta cell dysfunction occur concurrently. In this case, the major hormones involved in lipolysis and ketone body production would be catecholamines, cortisol, and growth hormone. We report a case of a 37-year-old female with a history of endocrine pancreatic insufficiency secondary to CP who presented with DKA, one of the life-threatening but preventable complications of diabetes. Noncompliance with insulin and concurrent urinary tract infection were the inciting factors. Her condition improved with DKA management according to standard protocol, intravenous antibiotics, and other supportive care. She got discharged after optimization of insulin therapy, with proper advice for home blood sugar monitoring and regular follow-up. A patient with pancreatic pathology may present to the emergency with DKA as the first manifestation, and if not properly evaluated, the diagnosis of type 3c diabetes can be missed.
RESUMEN
Imidacloprid is a neonicotinoid insecticide highly specific to nicotinic acetylcholine receptors in insects and other invertebrates. Nicotinic receptors in mammalian species have a low affinity to neonicotinoids. However, cross-reactivity with mammalian nicotinic receptors is a major concern especially due to the propensity of this commonly used agent to persist in environmental water sources for an extended period of time. Here, we present a case report of a patient who presented to the emergency department with features suggestive of neuromuscular junction dysfunction, following exposure to imidacloprid.
RESUMEN
Epilepsy can sometimes be mimicked in children by other organic conditions. We present a 11 year old boy with the congenital long QT syndrome who had recurrent "seizures" for five years which had been treated as epilepsy.
