Diseases of the pancreas csbrp

for Undergraduate Medical Students (MBBS)

1. Diseases of the
Pancreas
Dr.CSBR.Prasad, M.D.

2. Pancreas - Normal anatomy
Transversely oriented
Retroperitoneal
Extends from the duodenum to the splenic hilum
20 cm in length and weighs ~90 gm
Separated into four parts: (Based on adjacent
vasculature)
Head
Neck
Body &
Tail

3. Pancreas - Normal anatomy
The pancreatic duct system:
highly variable
Main pancreatic duct - Wirsung
Accessory pancreatic duct - Santorini
Ampulla of Vater - common channel for
biliary and pancreatic drainage - The main
pancreatic duct joins the common bile duct
proximal to the papilla of Vater

5. Greek word pankreas = “all flesh”
Lobulated organ
Two components: Exocrine & Endocrine
Exocrine portion – 80% to 85%
Endocrine portion – 1%
Pancreas - Normal anatomy

6. Exocrine portion:
Secretes inactive proenzymes
Trypsinogen
Chymotrypsinogen
Procarboxypeptidase
Proelastase
Kallikreinogen &
Prophospholipase A and B
Pancreas - Normal physiology

7. Endocrine portion:
1 million, islets of Langerhan
Secrete:
Insulin
Glucagon &
Somatostatin
Pancreas - Normal physiology

8. Self-digestion of pancreatic tissue is
prevented by several mechanisms:
Enzymes occur as inactive proenzymes
The enzymes are membrane-bound
Enterokinase is required for activation
Trypsin cleaves proenzymes
Trypsin inhibitors in acinar and ductal secretions
Acinar cells are resistant to many enzymes
Pancreas - Normal physiology

9. AGENESIS: PDX1 mutations on chromosome 13q
PANCREAS DIVISUM: Most common, 3% to 10%,
chronic pancreatitis
ANNULAR PANCREAS: 2
nd
portion of the
duodenum, duodenal obstruction
ECTOPIC PANCREAS : 2% of PMs, stomach and
duodenum, jejunum, Meckel diverticula, and ileum
Pancreas - Congenital Anomalies

11. Annular
pancreas

12. Pancreatitis
Inflammation of the pancreas
Injury to exocrine pancreas
Severity may range form mild self limiting
illness to life threatening acute
inflammatory process

13. Pancreatitis
Acute pancreatitis: Reversible
Gland returns to normal if underlying
pathology is removed
Chronic pancreatitis: Irreversible
By definition it’s irreversible loss of
exocrine parenchyma

14. Acute Pancretitis
Reversible pancreatic parenchymal injury
associated with inflammation
M:F = 1:3 (with biliary tract disease 6:1)
Biliary tract disease & gall stones account
for 80% of cases
Alcohol binge as precipitant – vary 60% in
some places to 5% in other areas

15. Etiologic Factors in Acute Pancreatitis
Metabolic
alcoholism
hyperlipoproteinemias
hypercalcemia
Drugs (azathioprine)
Genetic
Mutations in cationic tryprinogen and trypsinogen inhibitor gene
Mechanical
Gall stones
Trauma
Operative procedures
Vascular
shock
Atheroembolism
vasculitis
Infections
mumps

16. Etiologic Factors in Acute Pancreatitis –
less common causes
Ampullary carcinomas
Ascaris lumbricoides
Clonarchis sinensis
Hereditory pancreatitis

17. Hereditary Pancreatitis
Recurrent attacks of severe pancreatitis
Begins in childhood
Most of them are due to genetic mutations
Trypsinogen gets activated with in the
pancreas

18. Acute pancreatitis - Morphology
The basic alterations are:
Microvascular leakage causing edema
Necrosis of fat by lipolytic enzymes
Acute inflammation
Proteolytic destruction of pancreatic
parenchyma and
Destruction of blood vessels and subsequent
interstitial hemorrhage

20. Fat necrosis
Foci of fat necrosis may also be found in
extra-pancreatic collections of fat
Omentum
Mesentery of the bowel
Subcutaneous fat

21. Chicken soup exudate
In the majority of cases the peritoneal
cavity contains a serous, slightly turbid,
brown-tinged fluid in which globules of fat
can be identified
In its most severe form, hemorrhagic
pancreatitis, extensive parenchymal
necrosis is accompanied by dramatic
hemorrhage within the substance of the
gland

22. Red-black hemorrhage interspersed with
foci of yellow-white, chalky fat necrosis

24. Pathogenesis
Autodigestion of the pancreatic substance by
inappropriately activated pancreatic
enzymes

25. Pathogenesis
Inappropriate activation of trypsinogen is an
important triggering event in acute
pancreatitis

26. Pathogenesis
Inappropriate activation of Trypsin
With resultant activation of other
proenzymes
Prekallikrein (kinin system)
Hageman factor (Clotting, compliment sys)

27. Pathogenesis - Alcoholism
Alcohol consumption may cause pancreatitis
by several mechanisms:
1 - Secretion of protein-rich pancreatic fluid
2 - Increases pancreatic exocrine secretion
3 - Contraction of the sphincter of Oddi and
4 - Direct toxic effects on acinar cells

28. Clinical features:
1 Pain abdomen
2 Anorexia, nausea, and vomiting
3 leukocytosis, hemolysis, disseminated
intravascular coagulation,
4 Fluid sequestration
5 ARDS
6 diffuse fat necrosis.
7 Peripheral vascular collapse and shock
8 acute renal tubular necrosis

29. Lab findings:
1 Elevated Serum amylase (with in 24hrs)
2 Lipase (72hrs)
3 Glycosuria
4 Hypocalcemia (poor prognosis)

30. Macroamylasemia
Normal persons with high serum amylase
Because of large size they can not be
excreted in urine
May be mistaken for acute pancreatitis

31. Chronic Pancreatitis

32. Recurrent bouts of inflammation leads to
loss of pancreatic parenchyma and
replacement by fibrosis
Primary causes:
Alcohol abuse
Hypercalcemia / hyperlipoproteinemia
Pancreas divisum
Hereditary pancreatitis
Chronic Pancreatitis

33. Chronic Pancreatitis - Pathology
 Loss of lobular appearance of pancreas
Loss of exocrine tissue (typically not islets)
 Irregularly distributed fibrosis
 Reduced size of pancreas
 Inflammation
 Destruction of ducts – ductal dilatation
 Pseudocysts (25% of cases)

34. Chronic Pancreatitis - Gross
Normal
White areas of fibrosis

36. Chronic
Pancreatitis
- Micro
Normal

37. Sequelae - Acute Pancreatitis
 Systemic complications
Shock
Organ failure
 DIC
 Pancreatic abscesses
 Pseudocysts
 Duodenal obstruction

38. Sequelae - Chronic Pancreatitis
 Duct obstruction
 Pseudocysts
 Malabsorption (Steatorrhea, Vit deficiency)
 Secondary diabetes

39. Pancreatic Pseudocysts
 Localized collections of pancreatic
secretions (within or adjacent to pancreas)
 Virtually all arise after a bout of acute
or chronic pancreatitis
 Lack a true epithelial lining
Lined by macrophages, fibrosis
 Different from sterile pancreatic abscesses
Collections of neutrophils following liquefactive necrosis of
pancreatic parenchyma

40. Pancreatic Pseudocyst - Gross

41. Pancreatic Pseudocyst - Micro

42. Pancreatic Pseudocyst
vs. congenital
cyst

43. Cullen’s sign

44. Grey-Turner’s sign

47. E N D