Pancreatitis

Question 1

Describe the 2 components of pancreatic juice secreted by acinar, and duct and centroacinar cells.

Answer 1

Acinar cells - Low volume, viscous, enzyme-rich

Duct and centroacinar cells - High volume, water, bicarbonate rich

Question 2

What is acute pancreatitis essentially?

Answer 2

Autodigestion of pancreas due to pre-activated enzymes of digestion. Leads to rapid inflammation of pancreas.

Question 3

Why are enzymes released as zymogens initially from the pancreas?

Answer 3

Protects acini and ducts from auto-digestion.

Pancreas also contains a trypsin inhibitor to prevent trypsin activation.

Question 4

What enzyme do duodenal mucosa secretes and what does it do?

Answer 4

Enterokinase (enteropeptidase) which converts trypsinogen → trypsin.
Trypsin then converts all other proteolytic and some lipolytic enzymes into their active forms.

Question 5

Define chronic pancreatitis.

Answer 5

Long-standing inflammation of the pancreas.

Question 6

List all the causes of acute pancreatitis. (Aetiology)

Answer 6

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])

Question 7

Explain the pathogenesis of acute pancreatitis.

Answer 7

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.

Question 8

List the 3 different types of acute pancreatitis and briefly explain what each one is.

Answer 8

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.

Question 9

What are the symptoms of acute pancreatitis?

Answer 9

Fevers
Epigastric pain - radiating to back often eased by sitting forward.
N and V (vomiting +++)

Question 10

What are the signs of acute pancreatitis?

Answer 10

Haemodynamic instability (tachycardic, hypotensive)
Peritonism in upper abdomen OR generalised
Grey-Turner’s sign (bruising in flanks)
Cullen’s sign (bruising around umbilicus)

Question 11

Which specific type of pancreatitis are Grey Turner’s and Cullen’s signs seen in?

Answer 11

Haemorrhagic pancreatitis

Question 12

What differential diagnoses can be listed alongside a patient who has symptoms and signs of acute pancreatitis?

Answer 12

Gallstone disease and associated complications (e.g. biliary colic and acute cholecystitis)

Peptic ulcer disease/perforation

Leaking/ruptured AAA > aortic aneurysm

Question 13

List all the investigations that can potentially be done to confirm a diagnosis of acute pancreatitis.

Answer 13

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

Question 14

List causes of increase amylase levels.

Answer 14

Parotitis 
RF
Macroamylasaemia 
Bowel perforation 
Lung/ovary/pancreas/colonic malignancies can produce ectopic amylase.

Question 15

Outline the Modified Glasgow criteria for assessing severity of acute pancreatitis and how it is used.

Answer 15

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.)

Question 16

What are the 4 principles of management when it comes to acute pancreatitis?

Answer 16

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

Question 17

How do you manage patient who has a score, according to the Modified Glasgow criteria, indicative of severe acute pancreatitis?

Answer 17

Place them on high dependency unit (HDU).

Question 18

Should you use antibiotics in the management of patients with acute pancreatitis?

Answer 18

No, unless they have necrotic pancreatitis/infected necrosis.
(Antibiotics not given routinely).

Question 19

Is surgery ever required in the treatment of acute pancreatitis?

Answer 19

Yes, but rarely.

Question 20

List all the systemic complications of acute pancreatitis.

Answer 20

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

Question 21

List all the local complications of acute pancreatitis.

Answer 21

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)

Question 22

Outline the management of acute pancreatitis caused by an infected necrosis.

Answer 22

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).

Question 23

Explain what a pancreatic pseudocyst.

Answer 23

Peri-pancreatic fluid collection

Formation of a fibrous capsule encapsulating pancreatic enzymes (there is no epithelial lining).

Question 24

How long does pancreatic pseudocyst present after identification of pancreatitis?

Answer 24

6 weeks

Question 25

What % of pancreatic pseudocysts resolve spontaneously over 6 months?

Answer 25

95% and does’t require intervention

Question 26

In what scenarios would a pancreatic pseudocyst require surgical intervention?

Answer 26

Pseudocyst:

• symptomatic (Pain)
• causing compression of surrounding structures e.g. CBD (OJ), duodenum (small bowel obstruction) -
• infected (abscess)

Under these 3 circumstances, the pseudocyst is consequently drained.

Question 27

What does the management of a pancreatic pseudocyst involve?

Answer 27

Percutaneously under radiological guidance (CT)

Endoscopically - EUS puncturing of posterior wall of stomach and insertion of stent.

Surgically - laparoscopic/pseudocystgastronmy (cyst opened into stomach); pseudocystjejunostomy.

Question 28

What % of pancreas secretion is exocrine and what does it consist of?

Answer 28

98%

Secretes pancreatic juice into duodenum via MPD/sphincter of Oddi/ampulla > Digestive function

Question 29

What does chronic pancreatitis destroy?

Answer 29

Inflammatory process > destroys endocrine and exocrine tissue > fibrosis of pancreas

Question 30

What are the 2 major symptoms linked with chronic pancreatitis?

Answer 30

Insulin dependent DM

Steatorrhoea

Question 31

Outline how alcohol abuse leads to chronic pancreatitis.

Answer 31

Alcohol abuse > pancreatic juice - secretion of bicarbonate and fluid decrease > Proenzyme concentration + [citrate] and [lithostatin] decreased > Calcium salt precipitation

Both calcium precipitation and [proenzyme] increase leads to Ca2+ deposition leading to epithelial lesions and enzyme activation > Chronic inflammation and fibrosis of exocrine and endocrine pancreas

Question 32

List symptoms of chronic pancreatitis.

Answer 32

Pain (main symptom)
Malabsorption 
Weight loss 
Tissue atrophy 
Ductal stenosis 
Periductal fibrosis 
DM 
Pancreatic ascites 
Thrombosis of portal and splenic veins 
OJ 
Diarrhoea 
Pseudocysts

Question 33

Treatment of chronic pancreatitis

Answer 33

Recognise whether the patient is prescribed painkillers or diabetic medication → Pancreatic stone causing upstream back pressure within the pancreatic duct. Therefore endoscopist can insert stent to remove the stone through the AoV.

Surgical drainage - Removal of pus and necrotic tissue.

Surgical resection - Head/tail or entire pancreas removed → Phantom pain may arise.