[1] It can present as episodes of acute inflammation in a previously injured pancreas, or as chronic damage with persistent pain or malabsorption.

[5][6] Tobacco smoke and alcohol misuse are two of the most frequently implicated causes, and the two risk factors are thought to have a synergistic effect with regards to the development of chronic pancreatitis.

Type A involves intermittent, severe symptom flare-ups with or without objective pancreatitis separated by pain-free periods.

This includes mutations of the cystic fibrosis transmembrane conductance regulator (CFTR), serine protease inhibitor Kazal-type 1 (SPINK1), and the chymotrypsin C (CTRC) proteins.

[10] The mechanism of chronic pancreatitis viewed from a genetic standpoint indicates early onset of severe epigastric pain beginning in childhood.

R122H is the most common mutation for hereditary chronic pancreatitis with replacement of arginine with histidine at amino acid position 122 of the trypsinogen protein.

[5] The diagnosis of chronic pancreatitis is made based on the history and characteristics of symptoms combined with findings on radiologic imaging.

Symptoms of diarrhea, with oily, bulky, and foul-smelling stools indicated steatorrhea or fat malabsorption due to exocrine pancreatic insufficiency.

[11] Computed tomography, magnetic resonance cholangiopancreatography (MRCP), and endoscopic ultrasound (EUS) all have similar sensitivity and specificity for diagnosing chronic pancreatitis.

Medications such as pregabalin, gabapentin, tricyclic antidepressants and serotonin–norepinephrine reuptake inhibitors (SNRIs) are commonly used to treat pain in chronic pancreatitis.

[3] Alcohol cessation is important to manage pain and slow the calcific process, possibly reducing the future risk of flare-ups.