HPB Flashcards
Acute Pancreatitis Key Facts
Most common acute GI condition requiring hospitalization.
Severe cases can lead to necrosis, organ failure, or death.
Acute Pancreatitis Nutritional Risk
High catabolic rates → risk of malnutrition
Acute Pancreatitis Feeding Strategies
Mild AP: Start oral (PO) feeding early with a low-fat, soft diet once tolerated.
Severe AP: Use enteral nutrition (EN) within 24-72 hours to preserve gut integrity.
Parenteral Nutrition (PN): Reserved for cases where EN is contraindicated (e.g., bowel obstruction).
Acute Pancreatitis Formula Recommendations
Standard Polymeric: First-line for functional GI tracts.
Semi-Elemental: For malabsorption or intolerance to standard formulas.
Acute Pancreatitis Prohibited Substances:
Avoid probiotics in severe AP (no proven benefit, potential harm).
Avoid PERT unless exocrine insufficiency is confirmed.
Acute Pancreatitis Feeding Routes
Nasogastric (NG):
Preferred first-line: Easy placement, less invasive, and cost-effective.
Nasojejunal (NJ):
Indicated for digestive intolerance to NG feeding (e.g., vomiting, delayed gastric emptying).
Chronic Pancreatitis Pathophysiology
Progressive pancreatic inflammation → fibrosis and irreversible loss of function (endocrine & exocrine).
CP symptoms & complications
Symptoms: Severe abdominal pain, steatorrhoea, nausea, vomiting, diarrhoea, weight loss.
Complications: Pseudocysts, duct strictures, malnutrition, pancreatic exocrine insufficiency (PEI), type 3c diabetes (T3cDM).
Nutritional Recommendations in CP
- General Dietary Approach:
Well-nourished: Balanced, varied diet.
Malnourished: HEHP diet with 5-6 small meals/day. - Macronutrients:
Moderate-fat diet with PERT for digestion.
Focus on healthy fats (e.g., omega-3), restrict saturated fats. - Micronutrients:
Supplement fat-soluble vitamins (A, D, E, K), B12, iron, zinc, magnesium, selenium, and calcium. - Oral Nutritional Supplements (ONS):
Use when dietary intake is insufficient. - Bone Health:
Prevent osteoporosis with adequate calcium and vitamin D intake.
Perform DEXA scans every 2 years for at-risk patients.
Pancreatic Enzyme Replacement Therapy
Indications: Confirmed PEI.
Dosage:
Meals: 44,000–50,000 units lipase.
Snacks: 22,000–25,000 units lipase.
Administration Tips:
Take with meals/snacks and cold drinks.
Use PPIs to optimize effectiveness.
Avoid temperatures >25°C for storage.
Specialised Feeding Approaches in CP
Enteral Nutrition:
- Indicated for malnourished patients not responding to oral strategies.
- Use semi-elemental formulas if standard ones are poorly tolerated.
Parenteral Nutrition:
- Reserved for severe complications (e.g., gastric outlet obstruction).
- Administer via central venous access.
Management of T3cDM
Prevalence: 80% lifetime risk in CP patients.
Dietary Advice:
Regular meals with low-GI carbs; minimize sugary foods except for hypoglycaemic events.
Monitoring:
HbA1c every 6 months, regular blood glucose monitoring.
Consider CGMs for severe glycaemic instability.
FU & monitoring in CP
Nutritional Reviews: Regular assessment of weight, sarcopenia, deficiencies.
Biochemical Monitoring: Check fat-soluble vitamins, micronutrients, and markers of malabsorption.
Adjust PERT: Evaluate efficacy and address persistent maldigestion.
Bone Health: Regular DEXA scans for osteoporosis prevention.
CP Myths vs. Facts
Myth: Chronic pancreatitis is always caused by alcohol.
Fact: 20% of cases have non-alcoholic causes (e.g., genetic, autoimmune).
Myth: A low-fat diet is standard for CP.
Fact: Moderate-fat diets with PERT are now the standard.
Myth: Steatorrhoea only occurs with 90% pancreatic function loss.
Fact: Fat maldigestion can occur with less severe pancreatic damage.
Liver disease overview of stages
Compensated vs. Decompensated Cirrhosis:
- Compensated: Early stage; liver maintains function despite damage.
- Decompensated: Advanced stage; complications such as ascites, jaundice, and hepatic encephalopathy (HE) occur.
Cirrhosis: Late-stage scarring (fibrosis) due to liver diseases like hepatitis and chronic alcohol use.
Ascites: Fluid accumulation in the abdominal cavity, common in decompensated liver disease.