What is true regarding necrotizing pancreatitis: increased lipolysis, hypoglycemia, decreased gluconeogenesis, or protein synthesis?

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Necrotizing Pancreatitis: Metabolic Characteristics

The correct answer is A: Increased lipolysis occurs in necrotizing pancreatitis as part of the hypermetabolic and catabolic state that characterizes this severe inflammatory condition.

Metabolic Derangements in Necrotizing Pancreatitis

Hypermetabolic and Catabolic State

Necrotizing pancreatitis induces a profound hypermetabolic state with significant catabolism, which is a hallmark feature distinguishing patients who are "failing to thrive" from those recovering appropriately 1. This metabolic profile includes:

  • Increased lipolysis: Fat breakdown is accelerated as part of the systemic inflammatory response and energy mobilization 1
  • Increased gluconeogenesis (not decreased): The body generates glucose from non-carbohydrate sources to meet elevated energy demands 1
  • Protein catabolism (not synthesis): Muscle and tissue proteins are broken down rather than synthesized, contributing to the wasting seen in severe disease 1
  • Hyperglycemia (not hypoglycemia): Blood glucose levels are typically elevated due to stress response, increased gluconeogenesis, and insulin resistance 1

Clinical Significance of the Hypermetabolic State

The British Society of Gastroenterology specifically describes patients with necrotizing pancreatitis as requiring "continued system support with features of hypermetabolism and a catabolic state which suggest the development of complications" 1. This metabolic profile:

  • Indicates disease severity and potential for complications 1
  • Necessitates early nutritional support to counteract catabolism 2
  • Requires intensive monitoring in HDU/ICU settings 2

Nutritional Implications

The hypermetabolic and catabolic state directly informs management strategies:

  • Early enteral nutrition is essential to prevent gut failure and provide substrate for the elevated metabolic demands 2
  • Enteral feeding should be initiated via nasogastric or nasojejunal tube within 24 hours when tolerated 2
  • The goal is to counteract the protein catabolism and support the increased energy expenditure 2

Why Other Options Are Incorrect

Hypoglycemia (Option B): This is incorrect because necrotizing pancreatitis causes hyperglycemia, not hypoglycemia, due to stress-induced hormonal responses and increased gluconeogenesis 1.

Decreased gluconeogenesis (Option C): This is the opposite of what occurs; gluconeogenesis is actually increased to meet elevated energy demands 1.

Protein synthesis (Option D): Protein catabolism, not synthesis, predominates in the catabolic state of necrotizing pancreatitis 1.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Management of Necrotizing Pancreatitis

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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