Pancreatitis: Chronic
DEFINITION:
Chronic Pancreatic (CP) implies the presence of parenchymal fibrosis, and loss of glandular function
Marseilles-Rome/Sarles classification:
Lithogenic (Calcifying) CP: Largest group, ETOH is leading cause and is responsible for >70% of cases of chronic pancreatitis
Chronic calcifying pancreatitis; Irregular fibrosis of the pancreas with pancreatic duct stones & protein plugs, ductal injury
Obstructive CP: Intraductal tumor or benign ductal stricture in distal (tail end) of the gland;
Obstruction is not from stones
Glandular changes: uniform fibrosis, ductal changes with dilation, acinar atrophy; Often improves when obstruction is relieved
Inflammatory CP: Associated with autoimmune diseases such as Sjogren’s, PSC, autoimmune pancreatitis
Characterized histologically by mononuclear cell infiltration, associated exocrine parenchyma destruction, diffuse fibrosis, atrophy
Pancreatic Fibrosis: Also called Idiopathic Senile CP
Characterized by silent, diffuse perilobular fibrosis
Must rule out: nutritional/hereditary pancreatitis, hypercalcemia, trauma with duct injury, hyperlipidemia, autoimmunity, pancreatic divisum, obstruction, cancer
ETIOLOGIES: Other causes than those above:
Hereditary CP (High risk for pancreatic cancer):
Three genes have been associated with chronic hereditary pancreatitis:
Cationic Trypsinogen gene: cause autosomal dominant form of chronic pancreatitis (i.e. many family members)
Cystic fibrosis transmembrane conductance regulator (CFTR) and Pancreatic secretory trypsin inhibitor (SPINK1) genes
Mostly found in apparent sporadic forms of pancreatitis because they have low penetrance
Mesotrypsinogen gene is NOT implicated
Affects both ♂ & ♀ equally; Can present as acute pancreatitis in childhood by age 10-12
Cystic fibrosis: exocrine pancreatic insufficiency afflicts approximately 85% of CF patients
Reduced pancreatic duct secretions, leading to protein-rich acinar secretions becoming inspissated: proximal obstruction & fibrosis
PATHOPHYSIOLOGY:
Trypsin (inhibit) and Food (stimulate): CCK releasing peptide » pancreatic enzyme secretion » pain
CLINICAL MANIFESTATIONS/PHYSICAL EXAM:
Abdominal pain, Steatorrhea, Diabetes mellitus
Weight loss: decreased intake due to fear of pain, malabsorption, uncontrolled diabetes
Osseous abnormalities (5%): medullary infarcts or aseptic necrosis of femoral/humeral heads; From medullary fat necrosis during acute attacks
Nephrolithiasis: with steatorrhea, long-chain fatty acids bind to intraluminal calcium; Less calcium available to bind oxalate = more oxalate in urine
LABORATORY STUDIES:
Amylase and lipase not helpful: may be normal, elevated, or low
↓ Trypsin is suggestive of CP (although no serologic test is sensitive or specific for chronic pancreatitis)
Steatorrhea: must lose 90% of exocrine function before steatorrhea develops (takes 5-12 years); Pancreas has great reserve!
Fat soluble vitamin deficiency: although diminished, marked deficiency is UNcommon in chronic pancreatitis
Clinically easy bruising, bone pain, decreased night vision, is more suggestive of small bowel malabsorption, such as Celiac sprue
B12 malabsorption: cobalamin-binding proteins, usually destroyed by pancreatic enzymes, are binding more B12
Treat with pancreatic enzymes
DIAGNOSTIC STUDIES:
In later stages of the disease when calcifications and steatorrhea are present, the diagnosis is relatively straightforward
Difficulty arises if pancreatic structure and function are not unequivocally abnormal; Histology is standard, but often not available
KUB: focal or diffuse pancreatic calcification (30-40% of cases) makes the diagnosis of advanced CP, however not found in early CPRelated posts:
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