This document discusses tumours of the pancreas, including non-endocrine and endocrine neoplasms. It covers the incidence, risk factors, pathology, clinical features, investigations, management, and challenges with delayed diagnosis of pancreatic cancer. The main types of pancreatic tumours are discussed in detail, along with the surgical and non-surgical treatment options.

1. ‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬

2. TUMOURSOFTHEPANCREAS
Dr.
MOUSTAFA
HECAZY

3. The tumours of the pancreas can
be -
A. Non-Endocrineneoplasms
B. Endocrineneoplasms
TUMOURS OF THE PANCREAS

4. NON-ENDOCRINE NEOPLASMS:
 Benignnon-endocrineneoplasms of pancreas. Includes:-
(adenoma, cystadenoma, lipomas, fibromas,
haemingoma, lymphangioma and neuromas).
They are extremely rare and no clinical
significance unless they become palpable or
give pressure to adjacent structures and
cause symptoms. Can be solid or cystic or
both. The diagnosis should be made after
exclusion of more frequent malignant
tumours.

5.  Malignantnon-endocrineneoplasms. The most commonare:-
1. Ductal adenocarcinoma
2. Cystadenocarcinoma
NOTE: Periampullary carcinoma is term used for
juxta-pancreatic carcinomas. They are three
forms:-
 Carcinoma oftheampulla
 Carcinoma ofthelowerCBD
 Duodenalcarcinoma
Exocrine
cell of
pancreas

6. ENDOCRINE NEOPLASMS:
These are less common than non-endocrine
tumours and generally benign and sometimes
multiple. They includes:
 Insulinoma
 Glucogonomas
 Others:
- Gastrinomas
- Somatostatatinomas
- Vipomas (Vasoactive Intestinal
Polypeptide)
common

7. CARCINOMA
OF THE
PANCREAS

8. INCIDENCES:
Pancreatic cancer is the sixth leading cause of
cancer death in the UK.
Incidence is 10 cases per 100 000 population
per year.
Worldwide, it constitutes 2–3% of all cancers
In the USA, is the fourth highest cause of
cancer death.
The incidence has declined slightly over the
last 25 years.

9.  The exact causative factors
responsible are unknown. The peak
incidence in the 6th and 7th decade and
more in men than women.
The predisposing factors are:
 Diet (highprotein &highfat)
 Smoking
 Exposureto industrialcarcinogens
Contd…

10. Risk factors for pancreatic cancer development
Demographic factors
Age (peak incidence 65–75 years)
Male gender
Black ethnicity
Environment/lifestyle
Cigarette smoking
Genetic factors and medical conditions
Family history
Two first-degree relatives with pancreas cancer: relative
risk increases 18- to 57-fold

11. Germline BRCA2 mutations in some rare high-risk families
Hereditary pancreatitis (50- to 70-fold increased risk)
Chronic pancreatitis (5- to 15-fold increased risk)
HNPCC (hereditary non-polyposis colorectal cancer).
Ataxia telangiectasia
Peutz–Jeghers syndrome
Familial breast–ovarian cancer syndrome
Familial atypical multiple mole melanoma
Familial adenomatous polyposis – risk of
ampullary/duodenal carcinoma
Diabetes mellitus

12. Pathology
More than 85% of pancreatic cancers are ductal
adenocarcinomas.
The remaining tumours constitute a variety of
pathologies with individual characteristics.
Endocrine tumours of the pancreas are rare.
Ductal adenocarcinomas arise most commonly in
the head of the gland.
They are solid, scirrhous tumours, characterised
by neoplastic tubular glands within a markedly
desmoplastic fibrous stroma.

13. Fibrosis is also a characteristic of chronic
pancreatitis, and histological differentiation between
tumour and pancreatitis can cause diagnostic
difficulties.
Ductal adenocarcinomas infiltrate locally, typically
along nerve sheaths, along lymphatics and into blood
vessels.
Liver and peritoneal metastases are common.
Proliferative lesions in the pancreatic ducts can
precede invasive ductal adenocarcinoma.
These are termed pancreatic intraepithelial
neoplasia or PanIN, and can demonstrate a range of
structural complexity and cellular atypia.

14. Cystic tumours of the pancreas may be serous or mucinous.
Serous cystadenomas are typically found in older women, and
are large aggregations of multiple small cysts, almost like
bubblewrap.They are benign.
Mucinous tumours, on the other hand, have the potential for
malignant transformation.
They include: mucinous cystic neoplasms (MCNs) and
intraductal papillary mucinous neoplasms (IPMNs).
MCNs are seen in perimenopausal women, show up as
multilocular thick-walled cysts in the pancreatic body or tail and,
histologically, contain an ovarian-type stroma.
 IPMNs are more common in the pancreatic head and in older
men, but an IPMN arising from a branch duct can be difficult to
distinguish from an MCN
IPMNs arising within the main duct are often multifocal and
have a greater tendency to prove malignant.
Thick mucus seen extruding from the ampulla at ERCP is
diagnostic of a main duct IPMN.

15. Occasionally, lymphoepithelial cysts, lymphangiomas,
dermoid cysts and intestinal duplication cysts can show up
in the pancreas.
Solid pseudopapillary tumour is a rare, slowly
progressive but malignant tumour, seen in women of
childbearing age, and manifests as a large, part-solid, part-
cystic tumour.
Tumours arising from the ampulla or from the distal
common bile duct can present as a mass in the head of the
pancreas, and constitute around a third of all tumours in
that area.
Adenomas of the ampulla of Vater are diagnosed at
endoscopy as polypoid submucosal masses covered by a
smooth epithelium.
They can harbour foci of invasive carcinoma; the larger
the adenoma, the greater the risk.

16. Patients with familial adenomatous polyposis (FAP) can
present with multiple duodenal polyps.
Malignant transformation in a duodenal polyp is a
significant cause of mortality in these patients, mandating
endoscopic follow-up and pancreatoduodenectomy in
selected patients with high-grade dysplasia within the
polyp.
Ampullary adenocarcinomas often present early with
biliary obstruction.
Their natural history is distinctly more favourable
compared with pancreatic ductal adenocarcinoma.
Ampullary carcinomas are relatively small when
diagnosed, which may account for their better prognosis.
Occasionally, other malignant neoplasms can arise at the
ampulla, such as carcinoid tumours and high-grade
neuroendocrine carcinomas.

17. Spread of pancreatic tumours:
Ductal adenocarcinomas infiltrate by
A. Local Invasion
B. Lymphatic
C. Bloodvessels
D. Via peritoneal & omental causing ascites,Liver and
peritoneal metastases are common.

18. EVALUATION OF PANCREATIC NEOPLASMS:
 History
 ClinicalExamination
 Investigations
The specific investigations:-
 Ultrasound Scan  Histology & cytology
 CT Scan  Angiography
 MR Imaging  Laparoscopy
 ERCP

19. CLINICAL FEATURES:
 The diagnosis of pancreatic cancer
varies from the simple and clinically
obvious to the most difficult and
almost impossible the initial
symptoms and signs depend on the
site and extent of the pancreatic
cancer.

20.  Modes of presentation:
 Weight loss
 Pain
 Jaundice
 Steatorrhoea
 Diabetes Mellitus
 AcutePancreatitis
 Malignant Ascites
 Gastric Outlet Obstruction

21. •Jaundice secondary to obstruction of the distal bile duct is
the most common symptom that draws attention to
ampullary and pancreatic head tumours.
• It is characteristically painless jaundice but may be
associated with nausea and epigastric discomfort.
•Pruritus, dark urine and pale stools with steatorrhoea are
common accompaniments of jaundice.
•In the absence of jaundice, symptoms are often non-
specific, namely vague discomfort, anorexia and weight loss,
and are frequently dismissed by both patient and doctor.
•Upper abdominal symptoms in a recently diagnosed
diabetic, especially in one above 50 years of age, with no
family history or obesity, should raise suspicion.
•Occasionally, a patient will present with an unexplained
attack of pancreatitis; all such patients should have follow-
up imaging of the pancreas.

22. •Tumours of the body and tail of the gland often grow
silently, and present at an advanced unresectable stage.
• Back pain is a worrying symptom, raising the possibility of
retroperitoneal infiltration.
•On examination, there may be evidence of jaundice,
weight loss, a palpable liver and a palpable gall bladder.
•Courvoisier first drew attention to the association of an
enlarged gall bladder and a pancreatic tumour in 1890,
when he noted that, when the common duct is obstructed
by a stone, distension of the gall bladder (which is likely to
be chronically inflamed) is rare; when the duct is obstructed
in some other way, such as a neoplasm, distension of the
normal gall bladder is common.
•Other signs of intra-abdominal malignancy should be
looked for with care, such as a palpable mass, ascites,
supraclavicular nodes and tumour deposits in the pelvis.

23.  Approach to Investigations:
(Selective Investigations)
 Ultrasound Scan
 C.T. Scan
 MR Imaging Scan
 ERCP &EUS
 Histology & Cytology
 Angiography (Coeliac, Superior - Mesenteric)
 Laparoscopy

24. Investigation
In a jaundiced patient, the usual blood tests and ultrasound scan
should be performed.
 Ultrasound will determine whether or not the bile duct is dilated.
If it is, and there is a suspicion of a tumour in the head of the
pancreas, the preferred test is a contrast-enhanced CT scan.
In the majority of instances, this should establish if there is a
tumour in the pancreas and if it is resectable.
The presence of hepatic or peritoneal metastases, lymph node
metastases distant from the pancreatic head, encasement of the
superior mesenteric, hepatic or coeliac artery by tumour are clear
contraindications to surgical resection.
Tumour size, continuous invasion of the duodenum, stomach or
colon, and lymph node metastases within the operative field are not
contraindications.
 If the tumour minimally invades the portal or superior mesenteric
vein, not a contraindication to surgery (as part of the vein can be
resected), but complete encasement and occlusion of the vein is.

25. •MRI and MR angiography can provide information comparable to CT.
•ERCP and biliary stenting should be carried out if there is any
suggestion of cholangitis, if there is diagnostic doubt (small
ampullary lesions may not be seen on CT, and ERCP is the best way to
identify them) or if there is likely to be a delay between diagnosis and
surgery and the patient is deeply jaundiced with distressing pruritus.
It relieves the jaundice and can also provide a brush cytology or
biopsy specimen to confirm the diagnosis
•Otherwise, however, preoperative ERCP and biliary stenting is not
mandatory in patients with resectable disease; there is evidenc to
suggest that it is associated with a slightly higher incidence of
infective complications after surgery.
•The prothrombin time should be checked, and clotting
abnormalities should be corrected with vitamin K or fresh frozen
plasma prior to ERCP.
•If a stent is placed in a patient who may undergo resection, it should
be a plastic stent rather than a metal self-expanding one.

26. •EUS is useful if CT fails to demonstrate a tumour, if
tissue diagnosis is required prior to surgery (e.g. a
mass has developed on a background of chronic
pancreatitis and a distinction needs to be made
between inflammation and neoplasia), if vascular
invasion needs to be confirmed and in separating
cystic tumours from pseudocysts.
• Transduodenalor transgastric FNA or Trucut biopsy
performed under EUS guidance avoids spillage of
tumour cells into the peritoneal cavity.
•Percutaneous transperitoneal biopsy of potentially
resectable pancreatic tumours should be avoided as
far as possible.

27. • Histological confirmation of malignancy is desirable but
not essential, particularly if the imaging clearly
demonstrates a resectable tumour.
•The lack of a tissue diagnosis should not delay appropriate
surgical therapy.
• In patients judged to have unresectable disease, tissue
diagnosis should be obtained prior to starting palliative
therapy.
•Diagnostic laparoscopy prior to an attempt at resection can
spare a proportion of patients an unnecessary laparotomy
by identifying small peritoneal and liver metastases.
•It can be combined with laparoscopic ultrasonography.
•The tumour marker CA19-9is not highly specific or
sensitive, but a baseline level should be established; if it is
initially raised, it can be useful later in identifying
recurrence.

28. Carcinoma of the ampulla as
seen at endoscopy.
Same tumour (arrow) on
endoscopic ultrasound

29. A large ampullary adenoma that turned into an adenocarcinoma;
resection in the form of a pancreatoduodenectomy

30. ERCP can be utilized to:
detecting small tumors not visualized on CT (irregular solitary
duct stenoses >1cm long, abrupt cutoff of main pancreatic duct,
or panc and bile duct obstruction)
palliating biliary obstruction
brush cytology of the pancreatic duct has fair sensitivity (70%) but
excellent specificity
EUS can be utilized to:
aid in diagnosis and characterization of lesion
obtain tissue biopsy; may be associated with lower risk of
peritoneal seeding c/w percutaneous approach

31. DELAY IN DIAGNOSIS:
 Over 90% of patient with pancreatic cancer
present in the late stage of their disease. At
time no chance of cure.
 The factors responsible for late diagnosis
A. Tumour is asymptomatic in theearly stage.
B. Patient delay.
C. Physician delay.
D. Thepatient may not haveready and easy access to
competent diagnostic centre.

32. Is there a role for serum markers? If so, what?
CA 19-9 is a sialylated Lewis A blood group antigen commonly
expressed and shed in pancreatic and hepatobiliary disease, not
tumor specific
This antigen, when significantly increased, can assist in
differentiating between pancreatic adenocarcinoma and
inflammatory pancreatic disease, decrease in serial CA 19-9
correlates with survival of pancreatic patients after surgery or
chemotherapy
Debatable as to whether this is useful as early treatment of
recurrences have not been shown to improve outcomes

33. MANAGEMENT OF PANCREATIC CANCER:
A. Surgical Treatment
B. Non SurgicalTreatment

34. SURGICAL TREATMENT:
 Pancreatic Cancer is essentially
incurable since metastasis occurs at
such early stage. Any treatment must
be regarded as palliative.

35.  Surgical Options:
 For curative surgical treatment of
cancer in the head of pancreas the
optims are available:
A. Whipple operation (Pancreatico- duodenectomy)
B. PPPD Pylorus Preserving
Pancreaticoduodenectomy
C. Total Pancreatectomy
Contn…

36.  Palliative Surgical Treatment
(SurgicalBypass)
 For tail of the pancreas
(Distalpancreatectomy)
 Body of the pancreas
(Distal+ removal of the body of the
pancreas)

37. Management
•At the time of presentation, more than 85% of patients
with ductal adenocarcinoma are unsuitable for resection
because the disease is too advanced.
• If imaging shows that the tumour is potentially resectable,
the patient should be considered for surgical resection, as
that offers the only (albeit small) chance of a cure.
•If a cystic tumour is encountered, surgical resection should
be considered, as it carries a reasonable chance of cure.
•Tumours of the ampulla have a good prognosis and should,
if at all possible, be resected.
•Some of the rare tumours and the neuroendocrine lesions
should also be resected if at all possible.
•For those patients who have inoperable disease, palliative
treatment should be offered.

38. Surgical resection
•The standard resection for a tumour of the pancreatic head
or the ampulla is a pylorus-preserving
pancreatoduodenectomy (PPPD).
•This involves removal of the duodenum and the pancreatic
head, including the distal part of the bile duct.
•The original pancreatoduodenectomy as proposed by
Whipple included resection of the gastric antrum.
•Preserving the antrum and the pylorus is thought to yield a
more physiological outcome with no difference in survival or
recurrence rates.
•The Whipple procedure is now reserved for situations in
which the entire duodenum has to be removed (e.g. in FAP)
or where the tumour encroaches on the first part of the
duodenum or the distal stomach and a PPPD would not
achieve a clear resection margin.

39. •Total pancreatectomy is warranted only in situations
where one is dealing with a multifocal tumour (e.g. a main
duct IPMN), or the body and tail of the gland are too
inflamed or too friable to achieve a safe anastomosis with
the bowel.
•The PPPD procedure includes a local lymphadenectomy.
•Extended lymphadenectomy has not been shown to be
beneficial in improving survival and is associated with
increased morbidity.
•If the tumour is adherent to the portal or superior
mesenteric vein, but can still be removed by including a
patch or a short segment of vein in the resection, with an
appropriate reconstruction of the vessel, then that should
be done.

40. •For tumours of the body and tail, distal pancreatectomy
with splenectomy is the standard. Infiltration of the splenic
artery or vein by the tumour is not a contraindication to
resection.
•When removing the spleen, prior vaccinations against
pneumococci, meningococci and Haemophilus influenzae B
should be administered, and subsequent antibiotic
prophylaxis given .
•Attempts to downstage unresectable disease with
chemotherapy or chemoradiation and render it resectable
are rarely successful.
•Neoadjuvant chemotherapy or chemoradiation for
resectable disease should only be considered within a
clinical trial; it carries the risk that the disease may progress
despite the neoadjuvant therapy and become unresectable.

41.  Pre-operative preparation of the patient
for major surgery:
1. All jaundiced patients must be kept in good state of nutrition and
hydration.
2. Blood clotting deficiencies must be corrected.
3. Cardio pulmonary functioning carefully assessed.
4. Drainage procedureconsider in certain cases.

42. Pancreatoduodenectomy
•The clotting should be checked preoperatively and
adequate hydration ensured.
•The operation has three distinct phases:
• exploration and assessment;
• resection;
• reconstruction.
•A cholecystectomy is performed.
•The bile duct and hepatic artery are exposed, removing the
lymphatic tissue in this area.
• Exposure of the hepatic artery enables division of the
gastroduodenal artery and visualisation of the portal vein.
•The distal part of the gastric antrum is mobilised.
• The duodenum and right colon are mobilised from the
retroperitoneal tissues.

43. •The superior mesenteric vein is exposed inferior to the
pancreatic neck.
• Careful dissection into the plane between the vein and the
pancreatic substance will reveal whether the tumour is
adherent to the vein.
• The fourth part of the duodenum is dissected and freed
from the ligament of Treitz so that the upper jejunum can be
brought into the supracolic compartment.
• At this juncture, a decision has to be made whether to
proceed to the next phase of resection or not. If resection is
to be performed, the jejunum is divided 20–30 cm
downstream from the duodenojejunal flexure, and the
mesentery of the proximal jejunum is detached.
•The first part of the duodenum is divided.

44. •The neck of the pancreas is divided, and then the
uncinate process is separated from the superior
mesenteric artery and vein working up towards the upper
bile duct, which is divided, releasing the specimen.
•Retroperitoneal lymph nodes within the operative field
are completely removed with the specimen.
•Reconstruction is carried out.
•The pancreatic stump, the divided bile duct and the
duodenal stump are anastomosed on to jejunum, in that
order.
•Some surgeons prefer to anastomose the pancreas to the
posterior wall of the stomach instead; others prefer to
create a separate Roux loop of the jejunum and
anastomose the pancreas to that.
•The operation should take between 3 and 6 hours.

45. Adjuvant therapy
•The reported 5-year survival following resection of a
pancreatic adenocarcinoma ranges from 7% to 25%.
•The median survival is 11–20 months.
•Considering that, at best, 15% of patients have
resectable disease to begin with, this means only two
or three out of 100 patients with this disease can
expect to survive to 5 years.
• Moreover, recurrences can and do show up even
beyond the 5-year cut-off.
•It should be emphasised, however, that these
depressing statistics apply to ductal adenocarcinomas.
•Patients with resected ampullary tumours have a 5-
year survival of 40%, and cystic tumours and
neuroendocrine tumours can often be cured by surgical
resection.

46. •The high recurrence rate following resection has led to the
consideration of adjuvant treatments to improve outcome
•In a large multicentre European study ,adjuvant
radiotherapy or chemoradiotherapy was shown to confer no
advantage, but chemotherapy with 5-fluorouracil (5-FU)
provided an overall benefit (median survival with
chemotherapy was 20 months compared with 16 months
without).
•Further trials are in progress, using gemcitabine and 5-FU
in combination, and other agents.
•Most patients with resected ductal adenocarcinoma are
now offered adjuvant chemotherapy.
•Some centres continue to offer chemoradiotherapy, and
further trials of adjuvant chemoradiation are also in
progress.

47. Palliation of pancreatic cancer
Relieve jaundice and treat biliary sepsis
■ Surgical biliary bypass
■ Stent placed at ERCP or percutaneous transhepatic
cholangiography
Improve gastric emptying
■ Surgical gastroenterostomy
■ Duodenal stent
Pain relief
■ Stepwise escalation of analgesia
■ Coeliac plexus block
■ Transthoracic splanchnicectomy
Symptom relief and quality of life
■ Encourage normal activities
■ Enzyme replacement for steatorrhoea
■ Treat diabetes
Consider chemotherapy

48. Palliation
•The median survival of patients with unresectable, locally advanced,
non-metastatic pancreatic cancer is 6–10 months and, in patients
with metastatic disease, it is 2–6 months.
•If unresectable disease is found in the course of a laparotomy that
was commenced with the intent to resect, a choledochoenterostomy
and a gastroenterostomy should be carried out to relieve (or pre-
empt) jaundice and duodenal obstruction.
•The bile duct may be anastomosed to the duodenum, or to a loop of
jejunum.
•It is preferable to use the bile duct rather than the gall bladder.
•Cholecystojejunostomy is easier to perform, but the bile must then
drain through the cystic duct, which is narrow and, if the cystic duct is
inserted low into the bile duct, it is vulnerable to occlusion by tumour
growth.
• A coeliac plexus block can also be administered.

49. •A transduodenal Trucut biopsy of the tumour should be obtained.
•In patients found to have unresectable disease on imaging, jaundice
is relieved by stenting at ERCP .
•Stents may be made of plastic or self-expanding metal mesh.
•Plastic stents are cheaper but tend to occlude faster and, if the
patient is likely to have a longer life expectancy, a metal stent can be
used.
• If the patient is not a suitable candidate for endoscopic biliary
stenting, a percutaneous transhepatic stent can be placed .
•Obstruction of the duodenum occurs in approximately 15% of cases.
•If this occurs early in the course of the disease, surgical bypass by
gastrojejunostomy is appropriate but, if it is late in the course of the
disease, then the use of expanding metal stents inserted
endoscopically is preferable, as many of these patients have prolonged
delayed gastric emptying following surgery.
• If both biliary and duodenal metal stents are to be placed
endoscopically, the biliary one should be placed first.

50. •If no operative procedure is undertaken, an EUS-guided or
percutaneous biopsy of the tumour should be performed before
consideration of chemotherapy or chemoradiation.
The role of chemotherapy in the management of pancreatic cancer
remains ill defined. If the tumour is a lymphoma, then benefit is
without doubt.
•Lymphomas of the pancreas are rare and constitute less than 3% of all
pancreatic cancers.
•For patients with ductal adenocarcinoma, 5-FU or gemcitabine will
produce a remission in 15–25%, while the remainder will receive no
benefit from the therapy.
•No long-term cures have been described with chemotherapy or
radiotherapy.
•Steatorrhoea is treated with enzyme supplementation.
•Diabetes mellitus, if it develops, is treated with oral hypoglycaemics
or insulin as appropriate.
•Pain with either analgesics or an appropriate nerve block .

51. FUNCTIONING ENDOCRINE TUMOURS OF
THE PANCREAS:
 These are much less common than
adeno carcinoma. The beta cell
tumours secrete (Insulin) and called
INSULINOMAS. Another functioning
tumour secrete (Gastrin) called
GASTRINOMA which come from the
islets which cannot be classified
into either alpha or beta (non-beta).

52.  Other tumours are:
a. Vipoma (Werner-Morrisonsyndrome, Pancreatic cholera)
b. Somastatinoma
c. Glucagonoma
d. HPPoma(HumanPancreatic
Polypeptide tumours)
 Slow growing and therefore carry much
better prognosis.

53. INSULINOMA:
 The commonest islet cell tumour and arise
from the beta cell and situated anywhere
on the surface or within the substance
of the pancreas.
 Most tumours are benign adenomas but
15% are low grade carcinomas and
secrete (insulin).

54. How is insulinoma diagnosed?
• Whipple’s Triad:
• symptoms of hypoglycemia during fasting or exercise
• serum glucose <45mg/dL during symptoms
• relief of symptoms with administration of glucose
• Definitive test is 72-hour fast with measurement
of insulin and glucose
• 75% of patients develop symptoms and GB<40 within 24
hours
• insulin:glucose ratio >0.4 is indicative of insulinoma
• Elevated c-peptide proinsulin levels are
confirmatory along with screening for antiinsulin
antibodies, sulfonylureas

55. CLINICAL FEATURES:
Whipple described a triad of features
which typify the (insulinomas):
1. Fastingproduces fainting.
2. Duringthese “attacks”there is
hypoglycaemia.
3. The attacksmay be relieved by ingestionof
glucose.

56. INVESTIGATIONS:
1. Measurementof blood sugar in an attack.
2. Overnight fasting serumglucose and insulin level (before & after
overnight). Insulin level are estimated byradio- immunoassay.
3. Pre-operativelocalization of the tumour very important
identification at operation can be difficult.
[Combination CT Scan and selective angiography]

57. TREATMENT:
1. If the tumourlocalized surgical resection is the TR of choice
also this apply to metastases.
2. If the tumoursnot localized during surgery (Intra operative USS
can be done to localize thetumour) than resected.
3. Sub total distal resection for multiple tumoursis appropriate.
Contn…

58. 4. With negative exploration it is appropriate to perform
pancreatectomy distal to the superior mesenteric vessels.
5. The Hypoglycemic attacks may be relieved by diazoxide or
streptazotocin.

59. GASTRINOMA: (Zollinger-Ellison
Syndrome)
The tumour arising from the islets cell of
langhans in the pancreas and in the duodenal
wall.
The majority (60%) of these tumours are
malignant. They may be associated with (MEN
1) which are Parathyroid Hyperplasia, and
Pituitary Adenoma. Gastrinoma give rise to ZE
Syndrome which consist of triad
(hypersecretion of gastric acid, severe peptic
ulceration and the presence of non-beta cell
tumour of the pancreas or duodenum).

60. CLINICAL FEATURES:
 The disease present as peptic ulcer
disease in over 90%. They have typical
pain more severe and less response to
medical treatment.
 Co-existing diarrhoea.
 All complications of peptic ulcer disease
are present in (ZE-Syndrome) as acute
haemorrhage, perforation and recurrent
ulceration.

61. THE DIAGNOSIS OF ZE-SYNDROME:
 Severe peptic ulcerdisease doesn’t respond to
treatment.
 Multiplepeptic ulcersor ulcersin unusual locations such
as the distal duodenum or jejunum.
 Peptic ulcerdisease associated withdiarrhoea.
Contn…

62.  Recurrentpeptic ulcer disease following in acid reducing
operation (surgery).
 Peptic ulceris associated withMEN- 1 Syndrome.
 Markedelevation of serum gastrin.

63. TREATMENT:
 Medical therapy for control of the acid
hypersecretion in patient with ZE-
Syndrome Omprazole considered the
antisecretory drug of choice for all
gastrinoma patients.

64.  Surgical Treatment:
 Tumourexcision.
 Total gastrectomy.
 Patientwithmetastasesshouldhave medical therapy if
fail total gastrectomy.
 Gastrinomapatient withMEN1 Syndrome and
documented hyperparathyroidism should have
parathyroidsurgery performed prior to removal of
gastrinoma.