| What is chronic pancreatitis? | It is defined histologically as chronic irreversible damage of the pancreas, chronic inflammation, causing fibrosis (cell damage) and eventually duct and parenchymal damage (of pancreatic glands)
It can be defined clinically as abdominal pain + exocrine and endocrine insufficiency) |
| Suppose we have an alcoholic pt with acute pancreatitis, what should we expect? | We expect him to have chronic pancreatitis |
| Why is chronic pancreatitis a syndrome? | Since we can't obtain pancreatic tissue easily, we call it a syndrome with features including exposure to risk factors, genetic background, symptoms of exocrine and endocrine insufficiency, and structural changes of pancreas seen on imaging |
| What are the clinical presentations of chronic pancreatitis? | Abdominal pain (most common, occurs at beginning of the evolution and stops at the end, epigastric radiating to the back, may be associated with nausea and vomiting, and if severe causes loss of apetite)
Steatorrhea (no lipase activity, occurs when pancreatic enzyme secretion is less than 10% max output, get diarrhea and weight loss+ fat-soluble vitamin deficiency (A,E and D) and maybe osteoporosis and osteopenia, also caused by celiac disease)
DM (40-80% of pt, if we see pancreatic calcifications early onset and tail resection, less insulin -->give IV insulin) |
| What are the tests done for diagnosis of chronic pancreatitis? | Direct test (secretin-CCK (not used anymore))
Indirect test (fecal fat excretion most important and used, elastase in stool (not used in lebanon)) |
| What are the imaging findings of chronic pancreatitis? | On Xray (we see calcifications due to alcoholic pancreatitis (lethiasis of enzymes with calcium ions and thus close channels leading to necrosis, done laterally or obliquely on pt)
US not used
CT (sensitive and specific)
MRCP (best, see fibrosis of wirsung, we can see cavities due to acinar cell destruction by IV secretin admin where it fills the defect)
ERCP (we may see dilation, irregular path and calcifications)
EUS (detailed later) |
| What are the gradings of chronic pancreatitis by ERCP? | Cambridge grading (according to pancreatic duct and side branch involvement.
Normal, Equivocal (if main duct normal and <3 side are abnormal), mild (main normal and >3 side are abnormal), moderate (main abnormal and >3 side abnormal), severe (main abnormal with at least one of large cavity (>10mm), obstruction, filling defects, severe dilatation)) |
| What are the gradings of chronic pancreatitis seen on US or CT? | Normal
Equivocal (either mild dilation of duct, or gland enlargement)
Mild/Moderate (equivocal + >4mm dilatation or duct irregularity or cavities <10mm or parenchymal heterogeneity or focal necrosis)
Severe (mild + more severe cavities/ duct dilatation/ calcification/ obstruction...) |
| What are the observations of EUS in chronic pancreatitis? | See advanced chronic pancreatitis, imp since we see parenchyma not just the duct.
Highly accurate |
| When do we use hormonal stimulation test of pancreas? | In case all imagings are - done in a specialized center
Rk: ERCP not used diagnostically. |
| What are the etiologies of chronic pancreatitis? | Alcoholic Pancreatitis (50% of cases, even if acute he should stop since it will progress to chronic pancreatitis)
Smoking increases it alot, hypercalcemia, hyperTG are more for acute not chronic pancreatitis)
Genetics (hardly seen)
Autoimmune
Obstructive (not imp) |
| What is alcoholic pancreatitis? | occurs for men, 5 years of drinking 4-5 drinks per day + genetics + risk factors like smoking...
Many have an early phase of recurrent acute pancreatitis attacks which lasts 5 years and develops into chronic pancreatitis (abdominal pain recurrent attacks) |
| What are the treatment options of chronic pancreatitis? | Medical (analgesic (may get addicted), stop tobacco and alcohol, pancreatic enzyme and some somatostatin (octreotide))
Endoscopy (according to pathophysio, sphincterotomy, stent placement, duct stone removal)
Surgery (last option, open all wirsung (wirsungojejenostomy) |
| What are pseudocysts? | They occur in 25% of chronic pancreatitis pt, most commonly occurs with abdominal pain, persistent elevation of lipase enzyme, dx by imaging ez, complications occur for 20-40% of pt (include large peripancreatic vessels, infection, duodenum and stomach involvement, hemorrhage, fistula formation |
| What are the autoimmune pancreatitis? | They could cause acute or chronic pancreatitis, two types 1 and 2 differ on many aspects |
| What is the difference between autoimmune pancreatitis 1 and 2? | Histology (no damage of ductal epithelium in 1 while in 2 we have destruction)
IgG4 (present in type 1 and absent in 2)
Age (60-70 in 1 and 40-50 in 2)
Gender (male for 1 and both for 2)
Clinical presentation (more obstructive jaundice in 1 and more acute pancreatitis pain in 2)
Pancreatic imaging (more diffuse enlargment in 1 and more focal enlargement in 2)
Other organ involvement (more in 1 than 2)
other diseases (strictures, pseudotumors in 1 and IBD in 2)
Relapses (frequent in 1 and rare in 2) |
