1. Title: Pancreas.
Objectives: to
1. Describe shortly the anatomy , histology, and
embryology of pancreas.
2. Explain congenital anomalies of pancreas.
3. Study both acute and chronic pancreatitis.

2. Anatomy:
 From Greek word (pankreas) , meaning "all flesh“.
 Retroperitoneal organ extending from "C" loop of
duodenum to hilum of spleen .
 Divided into three parts: head, body, and tail.
 Main pancreatic duct (duct of Wirsung) drains
into duodenum at major papilla of Vater.

3.  Accessory pancreatic duct (duct of Santorini)
drains into duodenum through a separate minor papilla.
 In many adults, main pancreatic duct merges with
common bile duct thus creating ampulla of Vater.

4. Histology:
 Complex lobulated organ with distinct exocrine
and endocrine components.
 The exocrine portion: composed of acini
(produce enzymes needed for digestion), ductules
and ducts. it constitutes 80% to 85% of pancreas.
 The endocrine portion: composed of about 1 million
clusters of cells( islets of Langerhans); secrete insulin,
glucagon, and somatostatin. it constitute 1% to 2%
of pancreas.

5. PANCREAS Stained with H&E : 1 – acinus 2 - islet of Langerhans
3 - interlobular connective tissue septa 4 - blood vessels

6. Embryology:
 pancreas arises from fusion of dorsal
and ventral outpouchings of foregut.
o The majority of gland ( body, tail, superior/anterior
aspect of head, and accessory duct of Santorini )
is derived from dorsal primordium .
o Ventral primordium gives rise to posterior/inferior
part of head and duct of Wirsung .

7. Congenital Anomalies:
1. AGENESIS :
 Very rare, pancreas is totally absent (agenesis),
incompatible with life.
 The transcription factor IPF1 (PDX1) is critical
for development of pancreas.
 Germ line homozygous mutation in IPF1 gene on
chromosome 13 reported in these patient.

8. 2. PANCREAS DIVISUM:
 Clinically significant.
 Caused by failure of duct systems of dorsal and
ventral primordia to fuse.
 So bulk of pancreas (formed by dorsal primordium)
drains through duct of Santorini.
 Duct of Wirsung is very short and drains only small
portion of head of pancreas.

9.  Accumulated pancreatic secretions
predispose patients to chronic pancreatitis.

10. 3. ANNULAR PANCREAS:
 develops when one portion of ventral pancreatic
primordium becomes fixed, while other portion
is drawn around duodenum.
 When this portion fuses with head of pancreas,
it forms bandlike ring that completely encircles
second portion of duodenum .
 present with signs and symptoms of duodenal obstruction
such as gastric distention and vomiting.

11. 4. ECTOPIC PANCREAS :
 Found in 2% of routine postmortem examination.
 Favored sites are stomach and duodenum,
followed by jejunum, and ileum.
 Usually located in submucosa.
 Histologically: pancreatic acini , occasionally with islets
of Langerhans.
 May be visualized as a sessile mass.
 May cause pain from localized inflammation, or rarely
may cause mucosal bleeding.
 2% of islet cell tumors arise in ectopic pancreatic tissue.

12. Pancreatitis:
Acute pancreatitis:
 Reversible lesion.
 Ranging in severity from edema and fat necrosis ; to
parenchymal necrosis with severe hemorrhage.
Etiologic Factors :
Metabolic: Alcoholism, Hyperlipoproteinemia , and
Hypercalcemia.
Drugs: thiazide diuretics.
Genetic : mutation in genes encoding pancreatic enzymes
and their inhibitors [ trypsinogen (PRSS1) and
trypsin inhibitor (SPINK1) genes ].

13. Mechanical : Trauma , Gallstones , and
Iatrogenic injury (perioperative,
and endoscopic procedures )
Vascular:
Shock
Atheroembolism
Polyarteritis nodosa
Infectious:
Mumps
Coxsackie virus
Mycoplasma pneumoniae
Idiopathic : 10% to 20% of cases.

14. Morphology:
Gross: areas of red-black hemorrhage, with
foci of yellow-white chalky fat necrosis .
Microscope:
(1) microvascular leakage causing edema.
(2) fat necrosis by lipolytic enzymes.
(3) acute inflammatory reaction.
(4) proteolytic destruction of pancreatic parenchyma.
(5) destruction of blood vessels with subsequent
interstitial hemorrhage.

15. Acute pancreatitis: low power shows : hemorrhage, paranchymal
necrosis, fat necrosis , and acute inflammatory cells .

16. Pathogenesis:
 pancreatic enzymes present in acinar cells
in proenzyme form and have to be activated.
 Lysosomal hydrolases permitting proenzyme activation,
and local release of activated enzymes.
 Mechanisms of activation:
1. pancreatic duct obstruction.
2. primary acinar cell injury.
3. defective intracellular transport of proenzymes
within acinar cells.

17. Clinical Features and Diagnosis :
 Pain is constant and intense , often radiated to upper back.
 Systemic features due to release of toxic enzymes and
cytokines into circulation resulting in : leukocytosis,
hemolysis, DIC , ARDS, and diffuse fat necrosis.
 Peripheral vascular collapse and shock with
acute renal tubular necrosis due to profound fluid loss.

18. Lab. findings:
 Marked elevation of serum amylase levels during
first 24 hours, followed within 72 to 96 hours by
rising serum lipase level.
 Glycosuria: in 10% of cases.
 Hypocalcemia: result from precipitation of calcium soaps
in fat necrosis, if persistent it is poor prognostic sign.
 Direct visualization of enlarged inflamed pancreas
by radiographic means.

19. Treatment:
 Resting the pancreas by total restriction of
oral food and fluids intake.
 Supportive therapy.
Prognosis:
 Most patients recover fully.
 5% die from shock during first week of illness.
 ARDS and ARF are ominous complications.
 In surviving patients sequel include: sterile pancreatic
abscess and pancreatic pseudo cyst .

20. CHRONIC PANCREATITIS:
 Inflammation of pancreas with destruction of
exocrine parenchyma, and fibrosis.
 In late stages: destruction of endocrine parenchyma.
 Irreversible impairment in pancreatic function.
Etiology:
1. Most common cause is Long-term alcohol abuse.

21. 2. Less common causes include:
o Long-standing obstruction of pancreatic duct by:
calculi, trauma, neoplasms, or pancreas divisum.
o Tropical pancreatitis: in Africa and Asia, attributed
to malnutrition.
o Hereditary pancreatitis: germ line mutations in PRSS1 or
SPINK1 genes.
o Idiopathic: as in cystic fibrosis.

22. Pathogenesis: Four hypotheses:
1. Ductal obstruction by concretions:
accumulation of pancreatic enzymes.
2. Toxic-metabolic:
toxins including alcohol and its metabolites,
can exert direct toxic effect on acinar cells.
3. Oxidative stress:
Alcohol-induced oxidative stress may generate
free radicals in acinar cells.
4. Necrosis-fibrosis:
in hereditary pancreatitis autolysis-resistant trypsin
molecule causes acute pancreatitis, repeated episodes
of acute pancreatitis almost later develop chronic
pancreatitis.

23. Morphology:
Gross: pancreas is hard, sometimes with extremely
dilated ducts and visible calcified concretions.
Microscope:
 Parenchymal fibrosis.
 Reduced number and size of acini with sparing of
islets of Langerhans.
 Dilation of pancreatic ducts.
 Chronic inflammatory infiltrate around lobules and ducts.
 Ductal epithelium may be atrophied or hyperplastic
or may show squamous metaplasia.
 Islets of Langerhans become embedded in
sclerotic tissue, eventually they may too disappear.

24. Chronic pancreatitis : Markedly-diminished pancreatic parenchyma with relatively
increase in fattty tissue. The interstitimum: increases in fibrous component along
with chronic inflammatory cells.

25. Clinical Features and Diagnosis :
 Repeated attacks of mild or moderate abdominal pain,
or persistent abdominal and back pain.
 The disease may be entirely silent until pancreatic
insufficiency and diabetes mellitus develop.
 In others, recurrent attacks of jaundice or indigestion.
 Attacks may be precipitated by alcohol abuse, or
over eating .

26. Lab. Findings:
 Mild-to-moderate elevations of serum amylase.
 Elevation in serum levels of alkaline phosphatase.
 Visualization of calcifications within pancreas by
CT scan and US.
 Hypoalbuminemia and hypoalbuminemic edema from
malabsorption caused by pancreatic exocrine insufficiency .

27. Prognosis:
 Long -term outlook is poor, with mortality rate
over 20 to 25 years is 50%.
 Severe pancreatic exocrine insufficiency and chronic
malabsorption may develop, as can diabetes mellitus.
 Pancreatic pseudocysts develop in 10% of patients.
 Hereditary pancreatitis have 40% risk of developing
pancreatic cancer ; other forms predisposition is unclear.

28. Summary :
1. Pancreas is retroperitoneal organ divided
into three parts: head, body, and tail.
2. It has distinct exocrine and endocrine components.
3. Congenital anomalies include : Agenesis , divisum ,
annular , and ectopic pancreas.
4. Pancreatitis can be acute reversible, or chronic
irreversible lesion.

29. Questions:
1. Enumerate congenital anomalies of pancreas, and
write short notes on one of them?
2. Write short assay on pathogenesis of chronic
pancreatitis?
THANK YOU