Acute and Chronic

Pancreatitis
Objectives
• We will study
1. Pancreas – normal structure and
function
2. Acute Pancreatitis – pathogenesis,
presentation, investigation and
treatment
3. Chronic Pancreatitis – pathogenesis,
presentation, investigation and
treatment
Pancreas
Structure and Function
• Pancreas lies retroperitoneally across the
posterior abdominal wall from the second
part of duodenum to the spleen
• Pancreatic head is encircled by the
duodenum and tail is in contact with
spleen
• Pancreas has exocrine cells – 98% and
endocrine cells – 2%
Pancreas Anatomy – Structure and
Pancreas
• The main pancreatic duct joins the
common bile duct to enter the duodenum
as a single duct at the ampulla of valter

What is the importance?

• Gall stones or cholecystitis can cause
pancreatitis
Clinical presentation of Gallstones
Pancreas
Exocrine Function of Pancreas
• The pancreas Acinar cells produce
digestive enzymes – amylase, lipase,
colipase and proteases – Trypsinogen and
Chymotrypsinogen
Pancreas
Endocrine Function of Pancreas
• Hormone producing cells are islets of
langerhans secrete hormone
• There are five types of islets cells
1. Beta cells secrete insulin
2. Alpha cells secrete glucogan
3. D – Cells secrete Somatostatin
4. PP cells produce pancreatic polypeptide
5. Entrochromaffin cells produce serotonin
Pancreatitis
• Pancreatitis is divided into
1. Acute Pancreatitis
2. Chronic Pancreatitis

We will discuss each one

 Causes of
Acute Pancreatitis
Acute Pancreatitis
• It is acute inflammation of
pancreas, which occurs in
previously normal pancreas
and returns to normal after
resolution.
Pathogenesis of Acute
Pancreatitis
• It is due to activation of digestive enzyme
Trypsinogen to Trypsin within pancreas,
may be caused by rise in intracellular
Ca2+ which may trigger it
• May be due to impairment of Trypsin
degradation
• Activated enzyme Trypsin causes cellular
nacrosis
Pathogenesis of Acute
Pancreatitis
• Gall stones cause pancreatitis by blocking
pancreatic drainage at the level of
ampulla
• Alcohol – interferes with Ca2+ homeostasis
in pancreatic Acinar cells
Clinical Features of Acute
Pancreatitis
• Pain in epigastric region accompanied by
nausea and vomiting. Pain radiates to the
back.
• Inflammation spreads throughout the
peritoneal cavity.
• Involvement of retro peritoneum leads to
back pain.
Clinical Features of Acute
Pancreatitis
• Patient may give history of gall stones or
alcohol intake
• In severe cases, there may be
hypotension, tachycardia, and oligurea
Clinical Features of Acute
Pancreatitis
Abdominal examination
- May show tenderness and guarding and
reduced or absent bowel sounds

Specific clinical signs in severe

necrotizing
Pancreatitis
• Cullen signs – periumblical bruising
• Grey turner’s sign – flank bruising
Grey turner’s sign
Diagnosis of Acute
Pancreatitis
Blood test
• Serum amylase – increased three times more than
normal within 24 hours of onset of pain
Amylase falls back to normal in 3-5 days
• Serum Lipase – increased

• Urine amylase

Do other base line investigations

- Blood count, urea and electrolyte, blood glucose, liver
biochemistry, plasma calcium, arterial blood gases
- They help in assessing the severity of the attack
Diagnosis of Acute
Pancreatitis
Radiology
• Erect X-ray abdomen – to exclude
gastroduodenal perforation
• Supine abdominal film – may show gall
stones or pancreatic calcification
• Abdominal Ultrasound
- To look for gall stones in common bile
duct, dilated intrahepatic duct, also for
pancreatic swelling, nacrosis, and
peripancreatic fluid collection
Radiology (cont)
Contrast enhanced CT scan
• Should be performed after 72 hours to see for
pancreatic necrosis
• CT can detect fluid collection, abcess formation
and pseudocyst development
• MRI and MRCP (Magnetic Resonance
cholangiopancreatography) for pancreatic duct and
Biliary tree
• Endoscopic retrograde cholangiopancreatography
(ERCP) – used as treatment to remove the duct
stones in gall stone related pancreatitis
Pancreatitis
Assessment of Disease Severity
ACUTE PANCREATITIS – GLASGOW
CRITERIA
• P - PaO2 < 8kPa
• A - Age > 55 years
• N - Neutrophalia WBC > 15 × 109 /l
•C - Calcium < 2 mmol/l
•R - Renal function urea > 16 mmol/l
•E - Enzyme LDH > 600 iu/l, AST > 200 iu/l
•A - Albumin < 32g/l
•S - Sugar blood glucose > 10 mmol/l
• If patient score 3 or more, it indicates severe
pancreatitis and patient should be transferred to
ITU
Pancreatitis
Assessment of Disease Severity
• Majority of cases of pancreatitis are mild
and run short self limiting course
• But about 25% cases run complicated
course and 10% may be life threatening
• Increased CRP > 200mg/L in first four
days signifies severity
Abdominal CT showing swollen pancreas in acute pancreatitis
CT Abdomen showing pancreatic pseudocyst (Ps cyst)
Treatment
• IV fluids
• Nasogastric suction – prevents abdominal
distension and vomitus and decreases risk of
pneumonia
• Blood gases – will guide for O2 administration
• Antibiotic – Cefuroxime (reduces incidence of
pancreatic nacrosis)
• Analgesia – Pethidine or Tramadol
(Avoid morphine as it causes contraction of
sphincter of ODDI)
Long term outcome
• Mild and moderate cases of pancreatitis
usually make full recovery
• Severe acute pancreatitis may cause
pancreatic insufficiency. Both
exocrine (malabsorption) and
endocrine (diabetes).
CHRONIC PANCREATITIS
Chronic PancreatitisCauses of Chronic
Pancreatitis
• In developed countries, cause
of chronic pancreatitis is
alcohol in 60-80% cases.
• Other causes can be metabolic,
genetic, autoimmune
Chronic Pancreatitis
Pathogenesis
• Increased activated trypsin or impaired
clearance of trypsin
• Increased trypsin leads to precipitation of
protein within the pancreatic duct lumen in
the form of plugs and causes duct
obstruction
• Increase alcohol causes chronic pancreatitis
by impairing Ca2+ regulation which
promotes Trypsinogen activation to trypsin
Chronic Pancreatitis
Genetic aspect of chronic pancreatitis
• Genetic factors may be responsible for
trypsin activations e.g. cystic fibrosis
CFTR (cystic fibrosis transmembrane
conductance regulator) in apical surface
of Acinar cells

• Auto immune chronic pancreatitis (ACP)

There is increased IgG4 level, this
process is not dependent on trypsin
Chronic Pancreatitis
Clinical features
• Pain – epigastric region, radiates to the
back
• Anorexia and weight loss
• Exocrine and endocrine insufficiency
may develop i.e. malabsorption or
diabetes may be presenting feature
Investigation
• Serum amylase and lipase may be
increased
• Faecal elastase – abnormal (decreased) in
majority of cases of chronic pancreatitis
• Transabdominal ultrasound scan
• Contrast enhanced spiral CT-scan -
provides more assessment for
calcification in dilated pancreatic
duct
Contrast CT showing multiple calcification in
pancreas in Chronic Pancreatitis
Investigation
• MRI and MRCP (magnetic resonance
cholangiopancreatography)
• Endoscopic ultrasounds – for assessing
complication including pseudocyst
formation
• Diagnostic ERCP (endoscopic retrograde
cholangiopancreatography) – it has been
replaced by MRCP
Treatment of Chronic
Pancreatitis
• Chronic pancreatitis if alcohol related then
long term abstinence is advised
• For abdominal pain
- Opiate – Tramadol
- NASAID (Non steroidal anti-inflammatory
drugs)
- For chronic pain, amitryptyline (tricyclic
antidepressants)
- Stent of pancreatic duct to maintain duct
patency
Treatment of Chronic
Pancreatitis
• For Steatorrhea
- Pancreatic enzymes
- H2 – receptor antagonist or proton pump
inhibitors – to neutralize acidity in
duodenum

• Diabetes due to pancreatic disease may

need insulin
Complications of Chronic
Pancreatitis
• Pancreatic pseudocyst – (fluid collection
surrounded by granulation tissue)
If pseudocyst is < 6cm in diameter,
spontaneous resolution may occur
Pseudocyst can be drained
endoscopically, using endoscopic
ultrasound
Complications of Chronic
Pancreatitis
• Other complication of chronic pancreatitis
- Ascites
- Pleural effusion (rare) – increased
amylase in pleural fluid will confirm the
etiology
- Increased risk of cancer in chronic
pancreatitis
Additional Information
Clinical Syndromes - pancreas

• Insulinoma
• Gastrinoma
• VIPoma
• Glucagonomas
• Somatostatinomas
Insulinomas
• Insulinomas are pancreatic cell tumor,
derived from beta cells that secret insulin
• Classic presentation is fasting
hypoglycemia
• Other presenting feature may be
sweating, palpitation, weakness
• Diagnosis is confirmed by demonstration
of hypoglycemia with normal or elevated
insulin level
Gastrinoma

• There is hyper secretion of gastric acid

secondary to ectopic gastrin secretion
within endocrine pancreas – Zollinger -
Ellison Syndrome
• Patient has recurrent severe duodenal
ulceration
• Diagnosis is confirmed by elevated gastrin
level
• High dose proton pump inhibitors are
used to suppress the symptoms
VIPoma

• Endocrine pancreatic tumor producing

VIP (Vasoactive Intestinal Polypeptide)
• This causes severe secretary diarrhea due
to stimulation of Adenyl cyclase – Verner -
Morrison Syndrome (clinical syndrome
causing profuse watery diarrhea,
hypokalemia and metabolic acidosis)
Glucagonomas

• Glucagonomas are α-cell tumors

responsible for migratory necroletic
dermatitis, weight loss, diabetes mellitus,
deep vein thrombosis, anemia and
hypoalbumiaemia
• Diagnosis is made by measuring
pancreatic glucogan in the serum
Somatostatinomas
• Somatostatinomas are rare malignant D
cell tumors of the pancreas
• They cause diabetes mellitus, gall stones,
diarrhea, Steatorrhea
• They can be diagnosed by high serum
somatostatin level
Case History – Patient with
epigastric pain and weight loss
A 58 year old man presented to the medical
outpatient department with a 3 month history of
epigastric pain and 10kg in weight loss. Previously he
had been a heavy drinker but has cut back recently
due to his pain and vomiting. He gives history of
diarrhoea, passing pale and offensive stool 4-5 times a
day. He complains of marked thirst and nocturia.
On examination he looks dehydrated and unwell.
His pulse is 100/min, BP 110/60 mmHg. He smells
ketotic.
Abdominal examination – there is upper abdominal
tenderness, but no palpable mass, no organomegaly
and Ascites.
Blood test showed: Urine dipstick showed:
Hb 11.2 g/dL Ketones ++
MCV 105 fL Blood – ve
WCC 14.8 × 109/L Protein –ve
Platelet 380 × 109/L
Glucose 22.3 mmol/L
Na 128 mmol/L
K 3.1 mmol/L
Amylase 45 U/L
Case History – Questions:
1. His diarrhoea is most probably due to:
a. Continued alcohol consumption
b. Fat malabsorption
c. Lactose intolerance

2. Typical CT features of chronic pancreatitis include:

a. Pancreatic oedema
b. Pancreatic glandular calcification

3. Once his condition has been stabilized he will need

treatment with:
a. Oral hypoglycemic agents
b. Pancreatic enzyme supplements
c. Both a and b
Case History - Answers
Answer to Question 1:
b. Fat malabsorption
(Due to exocrine pancreatic insufficiency)

Answer to Question 2:
b. Pancreatic glandular calcification
(Calcification is feature of chronic pancreatitis. Oedema
is feature of acute pancreatitis)

Answer to Question 3:
c. Both a and b
(Pancreatic enzyme supplements and oral diabetic agents
will be needed in long term)
THANK YOU