Pancreas Flashcards
Diagnosis acute pancreatitis? (6)
Revised Atlanta classification and definitions: 2 of 3
• abdominal pain - persistent, severe epigastric pain which radiates to back
• serum lipase (preferred- more specific)/amylase activity of at least 3x greater than the upper limit of normal
• characteristic finings acute pancreatitis on CECT or MRI or trans abdominal US
• CT if:
- abdominal pain strongly suggest acute pancreatitis but amylase/lipase not high enough (may be the case in late presentation) to confirm diagnosis
-Local or late complications
- not responding to treatment so exclude other cause acute abdomen
Cause of mortality in acute pancreatitis? (2)
• Early phase: mods secondary to inflammatory cascade triggered by pancreatic parenchyma inflammation
• late phase > 2 weeks: secondary to septic complications ( infected necrosis)
Etiology acute pancreatitis? (12)
I get smashed
Idiopathic (3rd most common 15-25%)
Gallstones (most common 38%)
Ethanol (2nd most common 36%)
Trauma
Steroids
Mumps and other infections (CMV, mycoplasma, vzv)
Autoimmune: SLE, Sjogren’s syndrome (dry eyes dry mouth)
Scorpion toxin and other toxins
Hypercalcaemia, hypertriglycieridemia (metabolic causes)
Ercp (2-5%) -post ercp (endoscopic retrograde cholangiopancreatography)
Drugs (1-2 %): steroids, NSAIDs, diuretics, arvs esp stavudine
Rare causes: neoplasm (pancreatic or ampullary tumour), congenital (pancreatic divisum), genetics.
Treatment pancreatic pseudocyst as complication of acute pancreatitis?
Only treat if symptomatic- endoscopic cyst gastrostomy
Name 3 early local complications of severe acute pancreatitis
< 4 weeks after acute pancreatitis
• Acute peri-pancreatic fluid collection
• acute necrotic collection
• infected pancreatic necrosis (leading cause mortality)
Name 2 late local complications of severe acute pancreatitis
> 4 weeks after acute pancreatitis
• Pancreatic pseudocyst
• Walled-off necrosis
Treatment infected necrosis as complication of acute pancreatitis? (7)
• Empiric antibiotics known to penetrate pancreatic necrosis: carbapenems or quinolones (ciprofloxacin) and metronidazole
•step up approach necessary for lower complications:
1. Percutaneous radiologic guided drainage catheter
2. Catheter irrigated and upsized as needed
3. If no improvement in 72 hours- minimally invasive retroperitoneal approach video assisted retroperitoneal debridement VARD
4 endoscopic
5. Laparoscopic necrosectomy
6. Open surgical necrosectomy last resort
Treatment sterile necrosis as complication of acute pancreatitis? (4)
• Discontinue antibiotics and continue conservative treatment for 4-6 weeks
Only radiological/endoscopic/surgical if:
• ongoing gastric outlet, intestinal or biliary obstruction due to mass effect 4-8 weeks after onset acute pancreatitis
• persistent symptoms (eg abdominal pain, nausea, vomiting, anorexia) >8 weeks after onset
• disconnected duct syndrome (full transection pancreatic duct) with persisting symptomatic collections with necrosis (eg pain, obstruction ) >8 weeks after onset
Define chronic pancreatitis (4)
Irreversible, progressive disease with recurrent inflammatory episodes resulting in replacement of pancreatic parenchyma by fibrous connective tissue and ducal metaplasia.
This leads to progressive exocrine ( diarrhoea, steatorrhea) and endocrine (diabetes mellitus) pancreatic insufficiency
Imaging and features for Diagnosis chronic pancreatitis? (3)
• Early: endoscopic ultrasound - specific parenchymal and ductal features scored with rosemont criteria
. Calcifications = pathognomonic
• strictures main pancreatic duct : chain of lakes
Pathophysiology acute pancreatitis?
Unregulated activation trypsin within pancreatic acinar cells, activating pro-enzymes leading to auto digestion and inflammatory response. Can → sirs
How do gallstones cause acute pancreatitis? (2)
2 theories:
• obstructive theory - increased pressure pancreatic duct due to continuous secretion pancreatic juice in presence of pancreatic duct obstruction
. Reflux theory: stones impacted in ampulla of vater. Common channel forms that allows reflux bile salts into pancreas. Bile salts cause direct acinar cell destruction and necrosis.
How does alcohol cause pancreatitis? (4)
Triggers pro-inflammatory pathway pancreas
• increased expression and activity caspases (proteases that mediate apoptosis)
• decreased perfusion of pancreas
• sphincter of oddi spasm
• obstructs pancreatic ducts by precipitation of protein inside ducts
Symptoms acute pancreatitis? (5)
• Cardinal= epigastric and or peri-umbilical pain that radiates to back
• associated nausea and vomiting that doesn’t relieve pain
• dehydration, poor skin turgor, tachycardia, hypotension, dry mucous membranes common
Clinical presentation acute pancreatitis? (6)
• Mild pancreatitis: mild epigastric tender (but can have severe pancreatitis with mild findings)
. Severe pancreatitis: typically significant distention with generalised rebound tender and abdominal rigidity
• rarely: Grey turner sign (flank ecchymosis) and Cullen sign (peri-umbilical ecchymosis) - retroperitoneal bleeding associated with severe pancreatitis
• May have jaundice: concomitant choledocholithiasis or significant Edema of head of pancreas.
• May have dullness to percussion and decreased air entry in L (less commonly R) hemithorax. Pleural effusion secondary to acute pancreatitis.
Which sign is demonstrated by flank ecchymosis and may indicate severe acute necrotising pancreatitis?
Grey turner sign
Which sign is demonstrated by peri-umbilical ecchymosis and may indicate haemorrhagic pancreatitis?
Cullen sign
Name the 2 types acute pancreatitis
• Interstitial edematous pancreatitis: most patients. Diffuse enlargement secondary to inflammation and oedema. Clinical symptoms usually resolve within first week.
• necrotising pancreatitis:5-10% develop necrosis of pancreatic parenchyma or peri-pancreatic tissue or both. Variable history - may be solid or liquefy, sterile or infected, persist or disappear.