Pancreatitis Flashcards
Describe the 2 components of pancreatic juice secreted by acinar, and duct and centroacinar cells.
Acinar cells - Low volume, viscous, enzyme-rich
Duct and centroacinar cells - High volume, water, bicarbonate rich
What is acute pancreatitis essentially?
Autodigestion of pancreas due to pre-activated enzymes of digestion. Leads to rapid inflammation of pancreas.
Why are enzymes released as zymogens initially from the pancreas?
Protects acini and ducts from auto-digestion.
Pancreas also contains a trypsin inhibitor to prevent trypsin activation.
What enzyme do duodenal mucosa secretes and what does it do?
Enterokinase (enteropeptidase) which converts trypsinogen → trypsin.
Trypsin then converts all other proteolytic and some lipolytic enzymes into their active forms.
Define chronic pancreatitis.
Long-standing inflammation of the pancreas.
List all the causes of acute pancreatitis. (Aetiology)
GETSMASHED: Gallstones Ethanol Trauma Steroids Mumps and other viruses (EBV, CMV) Auto-immune (polyartheritis nodosa, SLE) Scorpion/snake bite Hypercalcaemia ERCP Drugs (SAND: steroids and sulphonamides, azothiopine, NSAIDs, diuretics [loop/thiazide])
Explain the pathogenesis of acute pancreatitis.
Increased permeability of pancreatic duct epithelium (alcohol, acetylsalicylic acid, histamine). Acinar cell enzymes diffuse into periductal interstitial tissue.
Pancreatic enzymes activated intracellularly: Proenzymes and lysosomal proteases incorporated into same vesicles → Trypsin activated → Autodigestion of acinar and ductal cells.
Alcohol precipitates and gallstones in ducts within AoV. Alcohol precipitates causes increase in upstream pressure due to obstruction, therefore causing bile to flow through the hepatopancreatic duct into the MPD → Irritations.
Reflux of duodenal contents: Activated enzymes through the AoV into the main pancreatic duct, trypsin activation of zymogens.
List the 3 different types of acute pancreatitis and briefly explain what each one is.
Haemorrhagic:
Elastase activity → Vascular arrosion and islet necrosis.
Oedematous:
Pancreatic enzymes trypsin, lipase and protease are activated within the duodenum under enterokinase activity. Activated enzymes are responsible for increased capillary permeability → permits volumes of fluid to pass into the peritoneal and retroperitoneal cavity. N.B. Characterised by interstitial inflammation and oedema.
Necrotic:
Necrosis of the pancreas resulting from ischaemia and vascular occlusion within the gland → Superseding infection → Infected necrosis.
What are the symptoms of acute pancreatitis?
Fevers
Epigastric pain - radiating to back often eased by sitting forward.
N and V (vomiting +++)
What are the signs of acute pancreatitis?
Haemodynamic instability (tachycardic, hypotensive)
Peritonism in upper abdomen OR generalised
Grey-Turner’s sign (bruising in flanks)
Cullen’s sign (bruising around umbilicus)
Which specific type of pancreatitis are Grey Turner’s and Cullen’s signs seen in?
Haemorrhagic pancreatitis
What differential diagnoses can be listed alongside a patient who has symptoms and signs of acute pancreatitis?
Gallstone disease and associated complications (e.g. biliary colic and acute cholecystitis)
Peptic ulcer disease/perforation
Leaking/ruptured AAA > aortic aneurysm
List all the investigations that can potentially be done to confirm a diagnosis of acute pancreatitis.
Blood tests: Amylase/lipase
X-rays: Erect CXR Abdominal XR (sentinel loop, gallstones)
USS (Ultrasound Scan):Look for gallstones as a cause for pancreatitis
CT abdomen: Patients not settling with conservative management and only 48-72 hours after symptom onset.
MRCP: If gallstones pancreatitis suspected with abdominal liver function tests (CBD stone)
ERCP: Remove CBD gallstones
List causes of increase amylase levels.
Parotitis RF Macroamylasaemia Bowel perforation Lung/ovary/pancreas/colonic malignancies can produce ectopic amylase.
Outline the Modified Glasgow criteria for assessing severity of acute pancreatitis and how it is used.
PO2 <8kPa Age >55 yrs White cell count >15 Calcium <2mmol/L Renal - urea >16mmol/L Enzymes - aspartate aminotransferase (AST) >200iu/L, lactate dehydrogenase (LDH) >600 iu/L Albumin <32g/L Sugar >10mmol/L
Score of 3 or more within 48 hours suggests severe acute pancreatitis.
(CRP is an independent predictor of severity >200 suggests severe pancreatitis.)
What are the 4 principles of management when it comes to acute pancreatitis?
Fluid resuscitation (IV fluids, urinary catheter, strict fluid balance monitoring).
Analgesia
Pancreatic rest (+/- nutritional support if prolonged recover → nasojejunal (NJ) tube feeding or total parenteral nutrition (TPN) feeding).
Determining underlying cause
How do you manage patient who has a score, according to the Modified Glasgow criteria, indicative of severe acute pancreatitis?
Place them on high dependency unit (HDU).
Should you use antibiotics in the management of patients with acute pancreatitis?
No, unless they have necrotic pancreatitis/infected necrosis.
(Antibiotics not given routinely).
Is surgery ever required in the treatment of acute pancreatitis?
Yes, but rarely.
List all the systemic complications of acute pancreatitis.
Hypocalcaemia (lipase → FFAs → Chelate Ca2+ salts leading to decrease in serum levels; process known as saponification)
Acute Renal Failure (ARF)
Systemic Inflammatory Response Syndrome (SIRS)
Hyperglycaemia
Adult Respiratory Distress Syndrome (ARDS)
Disseminated Intravascular Coagulation (DIC)
Multi Organ Failure (MOF) and death
List all the local complications of acute pancreatitis.
Pancreatic necrosis +/- infection (infected necrosis)
Pancreatic abscess
Pancreatic pseudocyst
Thrombosis of splenic vein, superior mesenteric vein, portal vein
Ascites
Small bowel venous congestion/ischaemia.
Haemorrhage → bleeding from eroded vessels
Small vessels → haemorrhagic pancreatitis (Cullen’s/Grey Turner’s sign)
Large vessels (e.g. splenic artery) → life threatening bleed (unless forms pseudo-aneurysm)
Chronic pancreatitis/pancreatic insufficiency (if recurrent attacks)
Outline the management of acute pancreatitis caused by an infected necrosis.
ABs + Percutaneous drainage
Infected pancreatic necrosis only indication for surgical intervention in the context of AP (High mortality if dead infected tissue isn’t removed).
Surgery involves necrosectomy (excision of necrotic tissue).
Explain what a pancreatic pseudocyst.
Peri-pancreatic fluid collection
Formation of a fibrous capsule encapsulating pancreatic enzymes (there is no epithelial lining).
How long does pancreatic pseudocyst present after identification of pancreatitis?
6 weeks
