| Revision as of 08:06, 18 December 2024 editSHAWNSHEARS (talk | contribs)74 edits -- Draft creation using the WP:Article wizard --Tag: Visual edit | Revision as of 08:22, 18 December 2024 edit undoSHAWNSHEARS (talk | contribs)74 editsNo edit summaryTag: Visual editNext edit → | ||
| Line 4: | Line 4: | ||
| == 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. --> | |||
Revision as of 08:22, 18 December 2024
 | Draft article not currently submitted for review.
This is a draft Articles for creation (AfC) submission. It is not currently pending review. While there are no deadlines, abandoned drafts may be deleted after six months. To edit the draft click on the "Edit" tab at the top of the window. To be accepted, a draft should:
It is strongly discouraged to write about yourself, your business or employer. If you do so, you must declare it. Where to get help
You can also browse Misplaced Pages:Featured articles and Misplaced Pages:Good articles to find examples of Misplaced Pages's best writing on topics similar to your proposed article. Improving your odds of a speedy reviewTo improve your odds of a faster review, tag your draft with relevant WikiProject tags using the button below. This will let reviewers know a new draft has been submitted in their area of interest. For instance, if you wrote about a female astronomer, you would want to add the Biography, Astronomy, and Women scientists tags. Add tags to your draft Editor resources
Last edited by SHAWNSHEARS (talk | contribs) 12 days ago. (Update) Submit the draft for review! |
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.