Acute and Chronic Pancreatitis, Disorders of the Exocrine Pancreas

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Scheme of Acute Pancreatitis Symptoms

Physiological Background

Under normal physiological conditions, pancreatic digestive enzymes are synthesized and secreted in inactive precursor (zymogen) forms to prevent autodigestion of the pancreas.

• Trypsinogen is activated to trypsin only after reaching the duodenum by the action of enteropeptidase (enterokinase) on the brush border of duodenal epithelial cells.
• Additional protective mechanisms include:
  • Packaging of enzymes in zymogen granules
  • Presence of pancreatic trypsin inhibitors (e.g., SPINK1)
  • Segregation of enzymes from the cytoplasm

Failure of these protective mechanisms results in pancreatitis.

Acute Pancreatitis

Definition and Pathogenesis

Acute pancreatitis is an acute inflammatory condition of the pancreas caused by premature activation of pancreatic digestive enzymes within the pancreatic parenchyma, leading to autodigestion of pancreatic tissue.

Early activation of trypsin plays a central role, as trypsin activates other digestive enzymes, including elastase, phospholipase A₂, and lipase.

This enzymatic activation results in:

• Acinar cell injury
• Autodigestion of pancreatic tissue
• Local and systemic inflammatory responses

Morphological Changes

The pathological consequences of enzyme activation include:

• Acute interstitial inflammation
• Fat necrosis (Balser’s necrosis)
  • Lipase-mediated digestion of peripancreatic fat
  • Free fatty acids bind calcium (saponification), producing chalky white deposits and contributing to hypocalcemia
• Hemorrhagic necrosis
  • Elastase-mediated destruction of blood vessel walls leading to hemorrhage
• Parenchymal liquefactive necrosis

Etiology

Common causes of acute pancreatitis include:

• Alcohol abuse
• Gallstones (cholelithiasis) causing pancreatic duct obstruction
• Trauma
• Post–Endoscopic Retrograde Cholangiopancreatography (ERCP)
• Hypercalcemia
• Hypertriglyceridemia
• Medications/Drugs
• Infections (e.g., Orthorubulavirus parotitidis – mumps virus)
• Autoimmune diseases (e.g., systemic lupus erythematosus)
• Certain scorpion venom
• Idiopathic

Clinical Features

Patients with acute pancreatitis typically present with:

• Severe upper abdominal pain radiating to the back
• Abdominal tenderness and guarding
• Nausea and vomiting
• Fever and tachycardia
• Leukocytosis

Laboratory Findings

Scheme of Acute Pancreatitis Complications

• Elevated serum amylase and lipase
• Hypocalcemia due to fat necrosis and saponification
• Elevated inflammatory markers (for example, CRP)

Complications

Severe acute pancreatitis may lead to:

• Infected pancreatic necrosis → sepsis
• Acute respiratory distress syndrome (ARDS)
• Disseminated intravascular coagulation (DIC)
• Hypovolemic shock
• Pseudocyst formation

Chronic Pancreatitis

Definition and Pathogenesis

Chronic pancreatitis is a progressive inflammatory disease characterized by irreversible destruction of pancreatic parenchyma, fibrosis, and impaired pancreatic function.

It most commonly develops as a consequence of recurrent episodes of acute pancreatitis, particularly in alcohol-related disease.

Scheme of Chronic Pancreatitis Symptoms

Pathological features include:

• Fibrosis
• Ductal distortion
• Calcifications
• Loss of acinar cells

Etiology

Causes of chronic pancreatitis include:

• Chronic alcohol abuse (most common)
• Genetic disorders
• Cystic fibrosis
• Hypercalcemia
• Hypertriglyceridemia
• Autoimmune pancreatitis
• Medications
• Idiopathic

Clinical Features

• Chronic or recurrent upper abdominal pain radiating to the back
• Nausea and vomiting
• Diarrhea
• Weight loss
• Exocrine pancreatic insufficiency
• Pancreatogenic diabetes mellitus
• Increased risk of pancreatic ductal adenocarcinoma

Laboratory Findings

In contrast to acute pancreatitis:

• Serum amylase and lipase are often normal or only mildly elevated
• This reflects advanced loss of acinar tissue and reduced enzyme production

Exocrine Pancreatic Insufficiency (EPI)

Definition and Pathophysiology

Exocrine Pancreatic Insufficiency (EPI) is a condition characterized by inadequate secretion of pancreatic digestive enzymes, resulting in maldigestion and malabsorption, particularly of fats.

Scheme of EPI symptoms

EPI commonly occurs in:

• Chronic pancreatitis
• Cystic fibrosis

In cystic fibrosis, thick mucus obstructs pancreatic ducts, preventing enzyme delivery to the intestine.

In chronic pancreatitis, progressive acinar cell destruction and ductal damage lead to reduced enzyme synthesis and secretion.

Clinical Features of EPI

• Steatorrhea (bulky, greasy, foul-smelling stools)
• Chronic diarrhea or constipation
• Abdominal discomfort
• Weight loss
• Fat-soluble vitamin deficiencies

References

1. Mayo Clinic Website: https://www.mayoclinic.org/diseases-conditions/pancreatitis/symptoms-causes/syc-20360227
2. NHS Website: https://www.nhs.uk/conditions/chronic-pancreatitis/
3. Stanford Health Care Website: https://stanfordhealthcare.org/medical-conditions/digestion-and-metabolic-health/chronic-pancreatitis/causes.html
4. Cleveland Clinic Website: https://my.clevelandclinic.org/health/diseases/21577-exocrine-pancreatic-insufficiency-epi
5. Robbins and Cotran Pathologic Basis of Disease, 10th Edition Kumar V, Abbas AK, Aster JC – Chapter: The Pancreas
6. Harrison’s Principles of Internal Medicine, 21st Edition – Sections on Acute and Chronic Pancreatitis
7. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 11th Edition – Pancreatic disorders