A.34 Chronic Pancreatitis

Question 1

A.34 Chronic Pancreatitis

Answer 1

Chronic pancreatitis is progressive inflammation with irreversible damage to pancreatic structure and function (both exocrine and endocrine).

Question 1

A.34 Chronic Pancreatitis
Etiology:

Answer 1

Main causes:
Alcohol abuse (60–70% of cases; especially men)
Pancreatic ductal obstruction (<10%; e.g., strictures from trauma or stones)
Tobacco use
Idiopathic pancreatitis (20–30%)
Hereditary pancreatitis (~1%; PRSS1 gene mutation, autosomal dominant, onset < 20 yrs)
Autoimmune pancreatitis
Systemic diseases:
- Severe hypertriglyceridemia (>1000 mg/dL)
- Primary hyperparathyroidism (hypercalcemia)
- Cystic fibrosis (~2% develop chronic pancreatitis)
Tropical pancreatitis: common in Tropics (esp. Southern India); young age at onset

Question 2

A.34 Chronic Pancreatitis
Pathophysiology

Answer 2

1. Autodigestion and Inflammation
   Damage to pancreatic acinar cells (e.g., alcohol)
   Outflow obstruction or premature activation of trypsinogen → trypsin
   Intraparenchymal activation of digestive enzymes (amylase, lipase)
   → Autodigestion of pancreatic tissue → Inflammation
2. Fibrosis
   Toxins/inflammatory mediators (e.g., alcohol, cytokines)
   → Activation of pancreatic stellate cells
   → Key contributors to pancreatic fibrosis
3. Pancreatic Insufficiency (from tissue atrophy + fibrosis)
   Exocrine insufficiency → ↓ lipase, amylase, protease
   → Malabsorption, steatorrhea, maldigestion
   Endocrine insufficiency → β-cell destruction
   → Pancreatic diabetes

Question 3

A.34 Chronic Pancreatitis
Clinical Features

Answer 3

1. Epigastric Abdominal Pain (main symptom)
   Radiates to the back, relieved by bending forward
   Worsens after eating
   Initially episodic, later becomes persistent
   Often with nausea and vomiting
   In late stages, pain may be absent
2. Features of Pancreatic Insufficiency
   Late manifestation (after ~90% of pancreas is destroyed)
   Exocrine insufficiency signs:
   Steatorrhea (fatty stools)
   Cramping pain, bloating, diarrhea, weight loss
   Can cause fat-soluble vitamin deficiencies (D, E, A, K)
   Malabsorption and weight loss
   Endocrine insufficiency signs:
   Pancreatic diabetes (due to β-cell destruction)

Question 4

A.34 Chronic Pancreatitis
Diagnostics (Imaging)

Answer 4

1. Abdominal CT (plain + contrast)
   Best initial test to screen for chronic pancreatitis
   Detects:
   Pancreatic atrophy
   Ductal dilations
   Ductal calcifications
   “Chain of lakes” appearance
   Can rule out pancreatic cancer or GI malignancy (esp. with epigastric pain + weight loss)
2. MRCP (Magnetic Resonance Cholangiopancreatography)
   Used when CT is equivocal but clinical suspicion is high
   Shows:
   Ductal strictures and dilations
   Pancreatic calcifications
3. Abdominal X-ray
   Shows visible pancreatic calcifications
   High specificity but low sensitivity (only seen in ~30% of cases)
4. Ultrasound (US)
   Abdominal US:
   Indistinct margins, pancreatic enlargement
   Calcifications, ductal dilation/strictures, or stones
   Endoscopic US:
   Parenchymal lobularity, hyperechoic foci
   Ductal dilation and calcification
5. ERCP (Endoscopic Retrograde Cholangiopancreatography)
   Detects early disease and allows treatment (e.g., duct stenting)
   Findings:
   Ductal stones (seen as filling defects)
   “Chain of lakes” / “string of pearls” (classic sign)
   Irregularity and dilation of main pancreatic duct

Question 5

A.34 Chronic Pancreatitis
Laboratory Tests:

Answer 5

1. Serum pancreatic enzymes
   Lipase = specific
   Amylase = non-specific
2. Pancreatic Function Tests
   Indirect tests:
   Fecal elastase-1 (FE-1):
   < 200 µg/g → pancreatic exocrine insufficiency
   < 100 µg/g → severe exocrine insufficiency
   72-hour fecal fat test:
   Fecal fat > 7 g/day = diagnostic for steatorrhea
   Direct tests:
   CCK test, secretin test, CCK-secretin pancreatic function test

Question 6

A.34 Chronic Pancreatitis
Genetic Testing:

Answer 6

Indications:
Family history of chronic pancreatitis
Young patients with idiopathic pancreatitis

Key genes:
PRSS1 mutation → hereditary pancreatitis
CFTR gene mutation → seen in ~40% of idiopathic cases

Question 7

A.34 Chronic Pancreatitis
Treatment:

Answer 7

Avoid alcohol and nicotine
Diet:
Small, regular meals
High in carbohydrates, low in fat
Supplement with medium-chain triglycerides
Pancreatic enzyme replacement (with meals)
Fat-soluble vitamins (DEAK) – parenteral if needed
Insulin for endocrine insufficiency

Pain Management
Analgesics:
NSAIDs, opioids (e.g., fentanyl, morphine)
Low-dose tricyclic antidepressants (e.g., amitriptyline)
For intractable pain:
Celiac ganglion block (temporary relief)
Endoscopic papillotomy + ductal dilation + stenting, stone removal
ESWL (extracorporeal shock wave lithotripsy) for intraductal stones

Surgical Management
Indications:

Suspected pancreatic cancer
Intractable pain not responding to other treatments
Procedures:
Pancreaticojejunostomy (if duct > 5 mm)
Partial pancreatectomy (e.g., Whipple’s procedure)
Thoracoscopic bilateral splanchnicectomy

Question 8

A.34 Chronic Pancreatitis
Complications:

Answer 8

1. Pancreatic insufficiency
   Due to fibrosis and acinar cell destruction
   Leads to malabsorption and pancreatic diabetes
2. Pancreatic pseudocysts
   Encapsulated fluid collections (develop ~4 weeks after acute attack)
   Occur in both acute and chronic pancreatitis
   Seen in ~10% of chronic cases

Wall is fibrous, not epithelial (unlike true cysts)

3. Splenic vein thrombosis
   Inflammation → thrombosis → left-sided portal hypertension
   → Risk of gastric varices
4. Pancreatic ascites
   Caused by:
   Ductal disruption (e.g., acute pancreatitis, trauma, surgery)
   Pseudocyst rupture
   → Leakage of pancreatic fluid → ascites
5. Other complications:
   Pancreatic abscess
   Portal vein thrombosis
   Pancreatic diabetes
   Pancreatic cancer (esp. in hereditary pancreatitis)