1. Acute and Chronic Pancreatitis
By Dr. Zahoor

2. Objectives We will study 1. Pancreas – normal structure and function
2. Acute Pancreatitis – pathogenesis,
presentation, investigation and treatment
3. Chronic Pancreatitis – pathogenesis,

3. 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%

4. Pancreas Anatomy – Structure and Functions

5. 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

6. Clinical presentation of Gallstones

7. Pancreas Exocrine Function of Pancreas
The pancreas Acinar cells produce digestive enzymes – amylase, lipase, colipase and proteases – Trypsinogen and Chymotrypsinogen

8. 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

9. Pancreatitis Pancreatitis is divided into 1. Acute Pancreatitis
2. Chronic Pancreatitis
We will discuss each one

10. Acute Pancreatitis It is acute inflammation of
Causes of
Acute Pancreatitis
Acute Pancreatitis
It is acute inflammation of
pancreas, which occurs in
previously normal pancreas
and returns to normal after
resolution.

11. 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

12. 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

13. 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.

14. 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

15. 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
Greyturner’s sign – flank bruising

17. Greyturner’s sign

18. 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

19. 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

20. 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

21. Pancreatitis
Assessment of Disease Severity

22. 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

23. 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

24. Abdominal CT showing swollen pancreas

25. CT Abdomen showing pancreatic pseudocyst (Ps cyst)

26. 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)

28. 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).

29. CHRONIC PANCREATITIS

30. Causes of Chronic Pancreatitis
In developed countries, cause
of chronic pancreatitis is
alcohol in 60-80% cases.
Other causes can be metabolic,
genetic, autoimmune

31. 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

32. 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

33. 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

34. 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

35. Contrast CT showing multiple calcification in pancreas

36. 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

37. 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

38. 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

39. 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

40. 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

41. Additional Information Clinical Syndromes - pancreas
Insulinoma
Gastrinoma
VIPoma
Glucagonomas
Somatostatinomas

42. 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

43. 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

44. 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)

45. 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

46. 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

47. THANK YOU