Pyla: Difference between revisions

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Latest revision as of 01:56, 17 February 2025

Pyloric Stenosis is a condition that affects the pylorus, the passage at the lower end of the stomach that leads into the small intestine. It involves the narrowing (stenosis) of the pylorus, which can significantly impact the movement of food from the stomach to the intestine. This condition is most commonly observed in infants and can lead to symptoms such as projectile vomiting, dehydration, and weight loss. The exact cause of pyloric stenosis is not well understood, but it is believed to involve a combination of genetic and environmental factors.

Symptoms and Diagnosis[edit]

The primary symptom of pyloric stenosis is projectile vomiting that occurs after feeding. The vomit does not contain bile. Infants may also show signs of hunger soon after vomiting and may have fewer and smaller stools due to the obstruction. Physical examination may reveal a palpable olive-shaped mass in the abdomen, which is the hypertrophied pylorus. Ultrasound is the preferred diagnostic method, as it can visualize the thickened pylorus.

Treatment[edit]

The treatment for pyloric stenosis is surgical and involves a procedure known as pyloromyotomy, which entails splitting the muscle of the pylorus to relieve the obstruction. This surgery is highly effective and is typically performed laparoscopically. Post-surgery, infants usually have a rapid recovery and can start feeding within hours after the procedure.

Epidemiology[edit]

Pyloric stenosis is more common in males than females, with a ratio of about 4:1. It typically presents in the first few weeks of life, most often between 2 and 8 weeks. There is also a genetic component, as the condition is more likely to occur in families with a history of pyloric stenosis.

Pathophysiology[edit]

The pathophysiology of pyloric stenosis is not completely understood. It involves the hypertrophy and hyperplasia of the muscles in the pylorus, leading to the narrowing of the gastric outlet. This results in obstruction of food passage from the stomach to the duodenum. The exact trigger for this abnormal muscle growth remains a subject of research.


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