The metabolic derangement in congenital pyloric stenosis is:
**Core Concept**
Congenital pyloric stenosis is a condition characterized by the narrowing of the pyloric channel, leading to gastric outlet obstruction. The metabolic derangement in this condition is primarily due to the inability of the infant to fully digest and absorb nutrients from the diet.
**Why the Correct Answer is Right**
The metabolic derangement in congenital pyloric stenosis is due to the excessive loss of hydrochloric acid (HCl) and gastric contents into the small intestine, leading to hypochloremic alkalosis. This occurs because the pyloric sphincter is unable to relax, allowing food to pass into the small intestine, where the HCl is absorbed, causing a decrease in serum chloride levels and an increase in serum bicarbonate levels. The body attempts to compensate for this loss by increasing renal bicarbonate reabsorption, leading to metabolic alkalosis.
**Why Each Wrong Option is Incorrect**
**Option A:** This option is not relevant to the metabolic derangement in congenital pyloric stenosis. The condition is not primarily related to a deficiency in pancreatic enzymes.
**Option B:** This option is incorrect because the metabolic derangement in congenital pyloric stenosis is not due to an excess of glucose in the blood. The condition is related to the loss of HCl and gastric contents, not glucose metabolism.
**Option C:** This option is incorrect because the metabolic derangement in congenital pyloric stenosis is not due to an excess of ketones in the blood. The condition is related to the loss of HCl and gastric contents, not ketone production.
**Clinical Pearl / High-Yield Fact**
In cases of congenital pyloric stenosis, the metabolic derangement can be managed with intravenous fluids and electrolyte replacement to correct the hypochloremic alkalosis. It is essential to monitor the infant's electrolyte levels and adjust the treatment plan accordingly.
**Correct Answer: A. Excessive loss of hydrochloric acid (HCl) and gastric contents into the small intestine, leading to hypochloremic alkalosis.**