Pyloric stenosis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The pathogenesis is not fully understood | |||
The gastric outlet obstruction due to the hypertrophic pylorus impairs emptying of gastric contents into the [[duodenum]]. As a consequence, all ingested food and gastric secretions can only exit via vomiting, which can be of a projectile nature. The vomited material does not contain [[bile]] because the pyloric obstruction prevents entry of duodenal contents (containing bile) into the stomach. | The gastric outlet obstruction due to the hypertrophic pylorus impairs emptying of gastric contents into the [[duodenum]]. As a consequence, all ingested food and gastric secretions can only exit via vomiting, which can be of a projectile nature. The vomited material does not contain [[bile]] because the pyloric obstruction prevents entry of duodenal contents (containing bile) into the stomach. | ||
Revision as of 13:50, 31 October 2017
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Pyloric stenosis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Pyloric stenosis pathophysiology On the Web |
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American Roentgen Ray Society Images of Pyloric stenosis pathophysiology |
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Risk calculators and risk factors for Pyloric stenosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
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Overview
Pathophysiology
The pathogenesis is not fully understood
The gastric outlet obstruction due to the hypertrophic pylorus impairs emptying of gastric contents into the duodenum. As a consequence, all ingested food and gastric secretions can only exit via vomiting, which can be of a projectile nature. The vomited material does not contain bile because the pyloric obstruction prevents entry of duodenal contents (containing bile) into the stomach.
This results in loss of gastric acid (hydrochloric acid). The chloride loss results in hypochloremia which impairs the kidney's ability to excrete bicarbonate. This is the significant factor that prevents correction of the alkalosis.[1]
A secondary hyperaldosteronism develops due to the hypovolaemia. The high aldosterone levels causes the kidneys to:
- Avidly retain Na+ (to correct the intravascular volume depletion)
- Excrete increased amounts of K+ into the urine (resulting in hypokalaemia).
The body's compensatory response to the metabolic alkalosis is hypoventilation resulting in an elevated arterial pCO2.
Associated Conditions
About 7% of babies will have other conditions such as intestinal malrotation, urinary tract obstruction, and esophageal atresia.
References
- ↑ Kerry Brandis, Acid-Base Physiology. Retrieved December 31, 2006.