Pancreatitis Flashcards
What are the components of pancreatic juice?
Low volume of viscous enzyme (protease, lipase, amylase) rich fluid - acinar cells
High volume of watery, bicarbonate rich fluid - duct and centroacinar cells
Problem for an organ making a cocktail of digestive enzymes is auto digestion -acute pancreatitis
Protection: proteases are released as inactive pro enzymes
Pancreas also contains trypsin inhibitor to prevent trypsin activation
Enzymes only activated in duodenum
Enterokinase converts trypsinogen to trypsin
Trypsin then converts all the other zymogen enzymes into their active forms
What are the definitions of acute and chronic pancreatitis?
Acute - rapid onset inflammation of the pancreas
Chronic - long-standing inflammation of the pancreas
What are the causes of acute pancreatitis (GET SMASHED)?
G - gallstones
E- ethanol (alcohol)
T- trauma
S- steroids
M- mumps and other viruses
A- auto immune (SLE)
S- scorpion/snake bite
H- Hypercalcaemia, hypertriglyceridaeimia, hypothermia
E- ERCP
D- drugs (SAND - steroids and sulphonamides, azothioprine, NSAIDS, diuretics)
What is the pathogenesis of acute pancreatitis?
Increased permeability of pancreatic duct epithelium (due to alcohol, acetylsalicylic acid, histamine)
-> Acinar cell enzymes diffuse into periductal interstitial tissue
Alcohol precipitates proteins in ducts (causes protein plug) -> increased upstream pressure
Pancreatic enzymes activated intracellularly
Pro enzymes and lysosomal proteases incorporated into same vesicles (for some reason. Usually they are put into different vesicles) -> trypsin activated
A gall stone could get stuck in the ampulla, leading to increased pressure in the pancreatic duct
Gall stone blocks ampulla, so bile flows from bile duct into pancreatic duct (bile reflux)
Reflux of duodenal content into pancreatic duct (activated enzymes)
What will extra or intracellular trypsin activation (inappropriate) lead to?
Activation of:
Phospholipase A2 -> hypocalcaemia
Elastase -> islet necrosis-> hyperglycaemia
Complement -> pancreatic gangrene
Prothrombin-> ischaemia -> pain
Kallikrein -> pain and shock
Systemic damage -> hypoxia and anuria
What are the types of acute pancreatitis?
Oedematous pancreatitis
Haemorrhagic pancreatitis
Necrotic pancreatitis (+/- superseding infection -> infected necrosis)
What are the signs and symptoms of acute pancreatitis?
Symptoms:
Epigastric pain radiating to back - often eased by sitting towards
Nausea and vomiting (esp vomiting)
Fevers
Signs:
Haemodynamic instability (tachycardia, hypotension)
Peritonism in upper abdomen/generalised
Grey-turners sign (bruising in flanks)
Cullens sign (bruising around umbilicus)
(Grey turners and cullens signs are seen in haemorrhagic pancreatitis)
What is a differential diagnosis for acute pancreatitis?
Gallstone disease and associated complications (e.g. biliary colic and acute cholecystitis)
Peptic ulcer disease/perforation
Leaking/ruptured
What investigation are done for acute pancreatitis?
Blood tests:
Amylase/lipase
(other causes of high amylase include renal Failure , bowel perforation, malignancies and others)
X rays:
Erect Chest x ray
Abdominal x ray (sentinel loop, Gall Stines)
Ultrasound:
Look for Gall stone as cause for pancreatitis
CT abdomen:
Patients not settling with conservative management and only 48 to 72 hours after symptom onset
MRCP:
If gallstones pancreatitis suspected with abnormal Liver function tests (CBD stone)
ERCP:
To remove CBD and bile stones
How do you assess the severity of acute pancreatitis?
Modified Glasgow criteria
P - PO2 <8KPa
A- age above 55
N- WCC >15
C- calcium below 2mmol/L
R- renal; urea above 16mmol/L
E- enzymes
A- albumin <32g/L
S- sugar above 10mmol/L
Score of three or more within 48 hours of onset suggests severe pancreatitis
CRO is an independent predictor of severity - above 200 suggests severe pancreatitis
How is acute pancreatitis managed?
Airway, breathing, circulation
4 principals of management include:
Fluid resuscitation
Analgesia
Pancreatic rest
Determining underlying cause
95% settle with concervative treatment
If severe pancreatitis on scoring -> high dependency unit
Antibiotics controversial -> commence if necrotic pancreatitis/ infected necrosis. But not routinely
Surgery only very rarely required
What are the systemic complications of acute pancreatitis?
Hypocalcaemia:
Lipase -> FFAs -> chelate Ca2+ salts -> decreased serum levels (saponification)
Hyperglycaemia (diabetes if significant beta cell damage)
Systemic inflammatory response syndrome
Acute renal failure
Adult respiratory distress syndrome
Disseminated intravascular coagulation
Multi organ failure and death
What are the local complications of acute pancreatitis?
Pancreatic necrosis +/- infection (infected necrosis)
Pancreatic abscesses
Pancreatic pseudocyst
Haemorrhage: due to bleeding from arroded vessels -
Small vessels -> haemorrhagic pancreatitis
Large vessels -> life threatening bleed
Thrombosis of splenic vein, SMV, portal vein
- > ascites
- > small bowel venous congestion/ischaemia
Chronic pancreatitis/pancreatic insufficiency
What is the management of infected necrosis?
Antibiotics and percutaneous drainage
Infected pancreatic necrosis only indication for surgical intervention in the context of acute pancreatitis
High mortality if dead infected tissue is not debrided
Surgery involves necrosectomy (excision of necrotic tissue)
What is a pancreatic pseudocyst?
Peri pancreatic fluid collection
Increase in concentration of pancreatic enzymes within a fibrous capsule
Presents more than 6 weeks after pancreatitis
95% spontaneously resolve over 6 months
Require no intervention unless:
Symptomatic (pain)
Causing compression of surrounding structures (eg. CBD -> obstructive jaundice)
Infected (abscess)
In these situations it is drained
