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| == Pathophysiology == | == Pathophysiology == | ||
| Colchicine's toxicity arises primarily from its mechanism of action, which involves binding to ] and disrupting ] formation, leading to impaired cellular processes. This disruption affects rapidly dividing cells, particularly in the ] and ], resulting in significant gastrointestinal symptoms such as ], ], and ] due to rapid turnover of intestinal mucosal cells. The drug is metabolized in the liver, primarily by ] enzymes, leading to the formation of several ], including 3-demethylcolchicine (3DMC) and 2-demethylcolchicine (2DMC). These metabolites can exhibit increased toxicity compared to the parent compound, contributing to ] injury and other systemic effects. As colchicine inhibits ] by preventing ] formation, it leads to multi-organ dysfunction. The early phase (10-24 hours post-ingestion) is characterized by gastrointestinal distress and initial ]. In the subsequent phase (24 hours to 7 days), patients may experience severe complications including ], ] (DIC), and cardiac issues due to direct toxicity on cardiac myocytes. The high affinity of colchicine for tissues like the liver and kidneys contributes to its rapid accumulation in these organs, leading to further complications. |
Colchicine's toxicity arises primarily from its mechanism of action, which involves binding to ] and disrupting ] formation, leading to impaired cellular processes. This disruption affects rapidly dividing cells, particularly in the ] and ], resulting in significant gastrointestinal symptoms such as ], ], and ] due to rapid turnover of intestinal mucosal cells. The drug is metabolized in the liver, primarily by ] enzymes, leading to the formation of several ], including 3-demethylcolchicine (3DMC) and 2-demethylcolchicine (2DMC). These metabolites can exhibit increased toxicity compared to the parent compound, contributing to ] injury and other systemic effects. As colchicine inhibits ] by preventing ] formation, it leads to multi-organ dysfunction. The early phase (10-24 hours post-ingestion) is characterized by gastrointestinal distress and initial ]. In the subsequent phase (24 hours to 7 days), patients may experience severe complications including ], ] (DIC), and cardiac issues due to direct toxicity on cardiac ]. The high affinity of colchicine for tissues like the liver and kidneys contributes to its rapid accumulation in these organs, leading to further complications. | ||
| == Symptoms == | |||
| Symptoms typically manifest in three phases: | |||
| === Phase 1 (10-24 hours) === | |||
| This initial phase is characterized primarily by gastrointestinal symptoms, which can be severe and debilitating. The most common early symptoms include nausea, vomiting, and abdominal pain, often intense and persistent. Diarrhea is another hallmark symptom, potentially becoming profuse and even ] in severe cases. These symptoms can lead to significant ] due to excessive fluid loss. patients may develop peripheral leukocytosis, an early increase in white blood cell count. This is often accompanied by electrolyte imbalances, including hyponatremia, hypocalcemia, and hypokalemia. The severe fluid loss and electrolyte disturbances can result in metabolic acidosis.<!-- Important, do not remove this line before article has been created. --> | |||
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Colchicine poisoning occurs due to the ingestion of colchicine, a drug derived from the plant colchicum autumnale, and can be life-threatening.
Pathophysiology
Colchicine's toxicity arises primarily from its mechanism of action, which involves binding to tubulin and disrupting microtubule formation, leading to impaired cellular processes. This disruption affects rapidly dividing cells, particularly in the gastrointestinal tract and bone marrow, resulting in significant gastrointestinal symptoms such as nausea, vomiting, and diarrhea due to rapid turnover of intestinal mucosal cells. The drug is metabolized in the liver, primarily by cytochrome P450 enzymes, leading to the formation of several metabolites, including 3-demethylcolchicine (3DMC) and 2-demethylcolchicine (2DMC). These metabolites can exhibit increased toxicity compared to the parent compound, contributing to hepatic injury and other systemic effects. As colchicine inhibits mitosis by preventing spindle formation, it leads to multi-organ dysfunction. The early phase (10-24 hours post-ingestion) is characterized by gastrointestinal distress and initial leukocytosis. In the subsequent phase (24 hours to 7 days), patients may experience severe complications including renal failure, disseminated intravascular coagulation (DIC), and cardiac issues due to direct toxicity on cardiac myocytes. The high affinity of colchicine for tissues like the liver and kidneys contributes to its rapid accumulation in these organs, leading to further complications.
Symptoms
Symptoms typically manifest in three phases:
Phase 1 (10-24 hours)
This initial phase is characterized primarily by gastrointestinal symptoms, which can be severe and debilitating. The most common early symptoms include nausea, vomiting, and abdominal pain, often intense and persistent. Diarrhea is another hallmark symptom, potentially becoming profuse and even bloody in severe cases. These symptoms can lead to significant dehydration due to excessive fluid loss. patients may develop peripheral leukocytosis, an early increase in white blood cell count. This is often accompanied by electrolyte imbalances, including hyponatremia, hypocalcemia, and hypokalemia. The severe fluid loss and electrolyte disturbances can result in metabolic acidosis.