acute and chronic pancreatitis

Question 1

acute pancreatitis epidemiology

Answer 1

35/100000, 5% mortality, 1st 2 weeks- systemic inflammatory response syndrome (SIRS), organ failure

SIRS- 2 or more abnormalities in the temp, heart rate, respiration, WBC, not related to infection

after 2 weeks - sepsis and its complication (infections)

Question 2

acute pancreatitis- gallstones

Answer 2

3-7 %of pateintws with gallstones develop acute pancreatitis, responsible for 35-40 % of cases - in sphincter of oddi

Ampulla obstruction due to stones, reflux of bile into the pancreatic duct–> edema from passage of a stone

Question 3

Acute pancreatitis- alcohol

Answer 3

10% of alcoholics develop acute pancreatitis, 30% of cases AP in the US
Usually after many year of alcohol abuse
not associated with binge drinking

Relaxation of sphincter–> duodenum enters pancreas, spasm of sphincer–> bile reflux, increased permeability of pancreatic duct, premature activation of enzymes

Question 4

Acute pancreatitis- hyper triglyceridemia

Answer 4

> 1000 gm/dl, 1-4% of AP cases, free fatty acid release- damages acini and capillary endothelium, lipemic serum

Question 5

Acute pancreatitis- pancreas divisum

Answer 5

There is a dorsal and ventral duct that fuse embryologically

Pancreas divisum the ducts never fuse and the main duct (dorsal) empties in the minor papilla

Question 6

acute pancreatitis genetic cause

Answer 6

serine protease 1 (PRSS1)
Hereditary pancreatitis (Autosomal Dominant)
Present in up to 80% of with hereditiarary pancreatitis unrelated to CF, Primary defense against pancreatitis is to control trypsin activity, either by prevention of premature activation of trypsinogen to trypsin, or by the destruction, inhibition or elimination of trypsin from the pancreas (mutation impairs this process)

Cystic fibrosis- CF transmembrane conductance regulator (CFTR), autosomal recessive, mutation may result in production of more concentrated or acidic pancreatic juice, leads to ductal obstruction or altered acinar cell function

Question 7

Acute pancreatitis pathogenesis

Answer 7

inflammation of the pancreas, similar cascade of events once pancreatitis begins after inciting event

Inciting event varies– early acute changes are similar–> systemic response are also similar

Question 8

Acute pancreatitis pathogenesis, early acute changes

Answer 8

Intraacinar activation of proteolytic enzymes- generation of large amounts of active trypsin within pancreas, vacuoules containing active trypsin rupture–> leading to further activation of trypsin and activation of chymotrypsin and elastase

Pancreatic autodigestion from intrapanccreatic release of active enzymes

Question 9

acute pancreatitis pathogenesis of early changes, results of pancreatic autodigestion

Answer 9

Microcirculatory injury- damage to vascular endothelium and acinar cells, decreased oxygen and ischemia

Inflammatory cytokines produced- Release of proinflammatory cytokines (TNF and interleukins)

Leukocyte chemoattraction- invasion by macrophages and PMN leukocytes

Increased vascular permeability and injury, induce thrombosis and hemorrhage –leading to pancreatic necrosis

Overwhelms normal protective mechanisms

Question 10

acute pancreatitis- systemic response

Answer 10

Systemic inflammatory response syndrome in the first 2 weeks (SIRS)
Acute REspiratory distress syndrome (ARDS)- phospholipase A digests lecithin, a major component of surfactant
Myocardial depression due to vasoactive peptides
Renal failure due to hypovolumia and hypotension
Bacterial translocation from gut due to compromised gut barrier (after the 1st 2 weeks)

Question 11

Acute pancreatitis clinical manfestations

Answer 11

acute onset of persistent, severe epigastric abdominal pain (some present without pain)

Pain radiates to the back- approximately 50%
Nausea and vomiting - 90% of patients
Illeus can be present

Cullens sign and grey turners sign– abdominal hemmorrhage in skin

Question 12

LAb finding s of acute pancreatitis

Answer 12

Amylase- elevated within 6-12 hours, short half life (10 hours)

Lipase- elevated within 4-8 hours, peaks at 24 hours, returns to normal in 2 weeks (LIPASE IS A BETTER diagnositc factor)

Elevation severeity does not equal severity of diseases
not helpful for prognsis

Question 13

acute pancreatitis diagnosis

Answer 13

presence of at least 2 of the following:

• Constant epigastric or right upper quadrant abdominal pain with radiation to the back, chest, or flanks
• Serum amylase and/or lipase>3 times the upper range of normal
• characterstic abdominal imaging findings (CAT scan)

Question 14

Acute pancreatitis complications

Answer 14

20% have local or systemic (renal, lung) complications

Local complications: acute peripancreatic fluid collection (<4 weeks)–> pseudocysts (>4weeks) (gastric comp)

Acute necrotic collection- infection

Question 15

acute pancreatitis treatment

Answer 15

Pain contorl, Aggressive IV fluids, antibiotic sfor infection
NUTRITION (give a few days off, then start on refeeding)

Address the underlying cause

ERCP- removal of the stone, mRCP- diagnostic injection

Question 16

chronic pancreatitis etiology

Answer 16

alcohol abuse, cigarrette, ductal obstruction, ampullary obstruction, genetic pancreatitis, Autoimmune pancreatiitts

Question 17

Chronic pancreatitis (CP), Pathogenesis

Answer 17

Progressive fibro-inflammatory process resulting in permanent structural damage (esp the pancreatic duct),

Diffeence between AP and CP-
AP usually painful, CP can be asymptomatic
Serum amylase and lipase can be noraml or only mild elevated
CP is patchy AP is diffuse

Question 18

Chronic pancreatitis path

Answer 18

increased pancreatic protein secretion–> plugs within ducts–> nidus for calcification–> stones within the ducts–> duct scarring and obstruction

Diagnosis - imaging og calcification and ductal dilatation, enlargement of the pancreas, fluid collections

Question 19

Chronic pancreatitis clinical anifestations

Answer 19

Pancreatic insufficiency- Fat malabsorption, DM , pain from pseydo cysts

bile duct/duodenal compression or infections from pseudocyts, increased risk of pancreatic adenocarcinoma

treatment- abstinence, analgesisc, diabetes, pancreatic enzyme supplementation, decompression of dilated pancreatic duct

Question 20

Autoimmune pancreatitis

Answer 20

IgG4- positive plasma cells in tissue, can affect multiple organs, can be both acute and chronic, treat with corticosteroids