Pancreatitis

Question 1

List some DDx for a presentation of:

• intermittent epigastric pain
• loose stools
• weight loss
• recurrent episodes over 3 yrs
• ETOH hx

Answer 1

• Pancreas- pancreatitis, pancreatic ca
• Gastric- gastritis, PUD perforation or haemorrhage, gastric ca
• Oesophagus- GORD, stenosis/stricture, malacia, oesophageal ca, variceal haemorrhage
• Hepatic- hepatitis, HCC
• Gallbladder- cholecystitis, cholelithiasis, cholangitis
• Aorta- AAA, aortic dissection
• Cardiac- angina, MI
• Respiratory- pneumonia (lower lobe) and sepsis
• GIT- SBO, appendicitis, coeliac disease

Question 2

List the causes of pancreatitis?

Answer 2

Pancreatitis causes (mnemonic I GET SMASHED):
I- idiopathic
G- gallstones
E- ETOH
T- trauma
S- steroids
M- malignancy/mumps
A- autoimmune
S- scorpion
H- hyperlipidaemia/ hypercalcaemia/ hyperparathyroidism
E- ERCP
D- drugs (e.g. Azathioprine/ immunosuppressant)

Question 3

List the risk factors for pancreatitis?

Answer 3

Risk factors:
• Gallstones
• ETOH
• Trauma (seatbelt, post-ERCP)
• SLE
• Genetic (CF, hereditary pancreatitis, AI pancreatitis)
• Medications (steroids, azithroprines, NSAIDs, diuretics)
• Metabolic (hypercalcaemia, raised TGs)
• Vascular (shock, atheroembolism)
• Infection (mumps, coxsackievirus, mycoplasma pneumonia)

Question 4

How is pancreatitis diagnosed?

Answer 4

Pancreatitis Dx criteria (requires 2/3):

1) Epigastric pain (assoc w nausea/vomiting, radiation to back)
2) Serum lipase (higher) or amylase > x3 normal range
3) Imaging: abdo US or CT showing pancreatic inflammation (peri-pancreatic fluid and fat stranding). Indicated when Dx unclear or no improvement.

Question 5

What imaging would you do for pancreatitis?

Answer 5

o Abdo US- diffusely enlarged, hypoechoic pancreas, pancreatic necrosis, peri-pancreatic fluid collections, pseudocysts. Help identify cause (e.g. gallstones)
o Abdo CT- peri-pancreatic fluid, fat stranding (lipase release damages surrounding fat)
o ERCP- if bile duct involvement suspected
o Abdo x-ray- paralytic ileus, calcification within/around pancreas (chronic)
o CXR- elevated hemidiaphragm, basal atelectasis (localised inflam), pleural effusion (3rd spacing), ARDS

Question 6

Explain the pathogenesis of the loose stools in pancreatitis?

Answer 6

Loose stools: due to fat malabsorption and mal-digestion
Path:
⇒ Fibrosis of fat parenchyma -> decreased acinar mass
⇒ Exocrine insufficiency (lipase, amylase, protease)
⇒ Reduced breakdown of fat (lipase), carbohydrate (amylase) and protein (protease)
⇒ Inability of intestines to absorbed derived micro-molecules
⇒ Increase fat content in stool -> steatorrhoea (>20g/day)

Question 7

Describe the differing effects of reduced lipase and amylase?

Answer 7

o Reduced lipase -> impaired fat metabolism -> steatorrhoea
o Reduced amylase -> impaired carb metabolism -> osmotic gradient across intestinal wall -> water dragged into intestine -> loose stools

Serum lipase x3 normal is Dx, better marker than amylase (elevation 7-10 days, more specific and sensitive), ETOH-hepatitis has lipase>amylase

Question 8

Describe the pathogenesis of weight loss in pancreatitis?

Answer 8

Weight loss- due to malabsorption, food avoidance and ETOH
1) Malabsorption path:
⇒ Exocrine insufficiency
⇒ Reduced breakdown of fat (lipase), carbohydrate (amylase) and protein (protease)
⇒ Inability of intestines to absorbed the derived micro-molecules
⇒ Decreased ability to meet metabolic caloric demands -> energy deficit
⇒ Catabolism of glycogen, fat and protein stores -> weight loss
2) Food avoidance- due to post-parandial pain (pancreatic enzyme release)
3) ETOH- impaired food intake

Question 9

Explain the pathogenesis of pancreatitis?

Answer 9

Path: premature activation of proteolytic enzymes (produced by pancreas, while still in pancreas) -> autodigestion
⇒ Defence systems overcome (pancreatic secretory trypsin inhibitor (PSTI)) -> large amount of trypsin inappropriately activated in pancreas
⇒ Rupture of acinar vacuoles containing pro-enzymes
⇒ Activation of more trypsinogen to trypsin
⇒ Activation of enzyme cascades -> production of amylase, trypsin, elastase and lipase -> cycle of cellular destruction
⇒ Activation of phospholipase and lipase-> fat necrosis
⇒ Elastase activation -> BV damage -> haemorrhage

Question 10

How can a gallstone cause pancreatitis?

Answer 10

⇒ Obstruction of pancreatic duct at ampullar of Vater (gallstone or localised oedema from passing stone)
⇒ Retrograde flow of pancreatic enzymes into pancreas
⇒ Pancreas irritation -> inflammation and uncontrolled pancreatic enzyme activation

Question 11

Explain ETOH-induced pancreatitis?

Answer 11

⇒ Acetaldehyde (ethanol metabolite) -> direct chemical injury to pancreatic ancinar cells -> pancreaitis
⇒ Acrinar cell injury -> activates pancreatic stellate cells -> increased production of collagen and other matrix proteins -> block ducts -> outflow duct obstruction -> pancreatitis

Question 12

What is saponification? What is seen on x-ray?

Answer 12

Enzymatic fat necrosis
⇒ Acinar cells -> release lipase -> release fatty acids from triglycerides
⇒ Complex with calcium -> form soaps
-> saponification (calcium salt + fat = soap)
⇒ Soaps appear as white chalky deposits on x-ray