This document provides an overview of diseases of the pancreas. It begins with the anatomy and physiology of the pancreas and then discusses specific diseases including diabetes mellitus, pancreatitis, neoplasms (benign and malignant tumors), cysts, and pseudocysts of the pancreas. For each disease, it provides details on causes, clinical presentation, diagnostic evaluation, and treatment. The document contains teaching slides with images, tables, diagrams and text to comprehensively cover various pancreatic diseases for educational purposes.

1. Dr. Mohammed
Hajhamad,
MB.ChB. M.S
Department of
Surgery
International
Medical School
MSU

2.  Introduction (anatomy and physiology)
 Diabetes mellitus
 Pancreatitis
 Neoplasms
 Benign
 Malignant
 Cysts and Pseudocysts
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3.  Gland with both exocrine and endocrine
functions.
 15-25 cm long
 60-100 g
 Location: retro-peritoneum, 2nd lumbar
vertebral level
 Extends in an oblique, transverse position
 Parts of pancreas: head, neck, body and tail
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8.  Rich periacinar network that drain into 5
nodal groups
 Superior nodes
 Anterior nodes
 Inferior nodes
 Posterior PD nodes
 Splenic nodes
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9.  Sympathetic fibers from the splanchnic
nerves
 Parasympathetic fibers from the vagus
 Both give rise to intrapancreatic periacinar
plexuses
 Parasympathetic fibers stimulate both
exocrine and endocrine secretion
 Sympathetic fibers have a predominantly
inhibitory effect
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10. Exocrine pancreas
 Trypsin
 Chymotrypsin
 Elastase
 Carboxypeptidase A
 Carboxypeptidase B
 Colipase
 Pancreatic lipase
 Cholesterol ester hydrolase
 Pancreatic α amylase
 Ribonuclease
 Deoxyribonuclease
 Phospholipase A
Endocrine Pancreas
 Insulin
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11.  Alpha cells produce glucagon.
 Beta cells produce insulin.
 Delta cells produce somatostatin.
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12.  Alpha cells secrete glucagon.
 Stimulus is decrease in blood
[glucose].
 Stimulates glycogenolysis and
lipolysis.
 Stimulates conversion of fatty
acids to ketones.
 Beta cells secrete insulin.
 Stimulus is increase in blood
[glucose].
 Promotes entry of glucose into
cells.
 Converts glucose to glycogen
and fat.
 Aids entry of amino acids into
cells.
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14.  Diabetes Mellitus is a chronic disorder of
carbohydrate, fat, and protein metabolism .
 In which there is impaired glucose
utilization due to defective or deficient
insulin secretory response inducing
hyperglycemia
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15.  Primary (idiopathic) Diabetes Mellitus
 Type-1 (Insulin Dependent Diabetes Mellitus)
 Type-2 (Non-insulin Dependent Diabetes
Mellitus)
 * Non-obese NIDDM
 * Obese NIDDM
 * Maturity onset diabetes of the young (MOD)
 * Gestational DM
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16. Insert table 19.6
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17.  Secondary (idiopathic) Diabetes Mellitus
 Chronic pancreatitis
 Post pancreatectomy
 Hormonal tumours (acromegaly, Cushing’s)
 Drugs (corticosteroids)
 Haemochromatosis
 Genetic disorders e.g. lipodystrophy
 Gestational DM
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18.  By far the most common in Malaysia and
worldwide.
 Type 1 and type2 have different pathogenesis
and metabolic characteristics.
 Similar long term complications occur in both
types.
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19.  Young
 Rare
 Linked to chrom. 7 & 20
 Autosomal dominant
 Mild hyperglycemia
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20. 1. Diabetic Ketoacidosis coma (DKA)
 In Type I Diabetes Mellitus
 Due to severe insulin deficiency with increase
glucagons
2. Non ketotic Hyperosmolar Coma
 In Type II DM (NIDDM)
 Elderly
 Uncontroled DM
Sustained hyperglycemic diuresis 
Severe dehydration  coma
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21.  Depends on :
 - Duration
 - Metabolic control
 - Genetic factors
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22.  Microangiopathy:
Thickening of basement membrane
 - Renal Glomeruli nephropathy
 - Retina retinopathy
 - Nerves neuropathy
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23.  Atherosclerosis:
 - Myocardial infarction
 - Cerebral stroke .
 - Aortic aneurysm .
 - Gangrene of lower extremities
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25.  Neuropathy:
 - Symmetric peripheral neuropathy .
 - Sexual impotence .
 - Bowel and bladder dysfunction.
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26.  Change in lifestyle:
 Increase exercise:
 Increases the amount of membrane GLUT-4 carriers in
the skeletal muscle cells.
 Weight reduction.
 Increased fiber in diet.
 Reduce saturated fat
 Pharmacotherapy, insulin and oral agents
 Surgery, pancreatic transplant and bariatric
surgery.
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28.  Inflammatory process in the pancreas
Types:
1. Acute pancreatitis
2. Acute relapsing pancreatitis
3. Chronic relapsing pancreatitis
4. Chronic pancreatitis
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29.  Common Causes
 Gallstones (including microlithiasis)
 Alcohol (acute and chronic alcoholism)
 Hypertriglyceridemia
 Endoscopic retrograde cholangiopancreatography
(ERCP), especially after biliary manometry
 Trauma (especially blunt abdominal trauma)
 Postoperative (abdominal and nonabdominal
operations)
 Drugs (azathioprine, 6-mercaptopurine,
sulfonamides, estrogens, tetracycline, valproic acid,
anti-HIV medications)
 Sphincter of Oddi dysfunction
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30.  Uncommon Causes
 Vascular causes and vasculitis (ischemic-hypoperfusion
states after cardiac surgery)
 Connective tissue disorders
 Thrombotic thrombocytopenic purpura (TTP)
 Cancer of the pancreas
 Hypercalcemia
 Periampullary diverticulum
 Pancreas divisum
 Hereditary pancreatitis
 Cystic fibrosis
 Renal failure
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31.  Abdominal pain
 Vomiting
 Nausea
 Lethargy
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32.  Grey Turner sign  Cullen’s sign
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33.  Requires two of the following:
 typical abdominal pain,
 threefold or greater elevation in serum amylase
and/or lipase level,
 and/or confirmatory findings on cross-sectional
abdominal imaging.
Plain X-ray
USG
CT Scan
MRI
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34.  IV fluids
 Analgesia
 Supportive management
 Surgery
- to relieve biliary obstruction
- to drain collection
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36.  Benign v/s malignant
 Exocrine v/s Endocrine ( Pancreatic islet cell
tumors )
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37. Cell Hormone Tumor
 Alpha cell Glucagon Glucagonoma
 Beta cell Insulin Insulinoma
 Delta cell Somatostatin Somatostatinoma
 Delta-2-cells VIP WDHA
(Vipoma)
 G-cells Gastrin ZES (Gastrinoma)
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38.  Usually diabetic patient
 Weight loss
 Dermatitis
 Anemia
 Stomatitis
 70% malignant
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39.  Peptic ulceration
 Abdominal pain
 Diarrhea
 GI bleed
 Perforation of ulcer
 Dehydration and malnutrition
 Diagnosis: 12 hour overnight acid output and
increased serum gastrin
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40.  They are adenomas, 90% benign 10%
malignant.
 Whipple’s triad
- episodes of illness precipitated by fasting
- hypoglycemia
- relief of symptoms by oral or intraveinous
glucose.
 Diagnosis: fasting insulin and glucose levels
 Treatment: surgical, resection of tumor,
medical for incurable patients or malignant
disease.
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41.  Adenocarcinomas
 Most common pancreas tumor
 Etiology unknown
 Risk factors
 Cigarette smoking
 High intake animal fat and meat
 Chronic pancreatitis
 Several hereditary disorders
 Hereditary pancreatitis
 Von Hippel-Lindau syndrome
 Lynch-syndrome
 Ataxiatelangiectasia
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42. Symptoms:
 Early non-specific
 Anorexia
 Weight loss
 Abdominal discomfort
 Nausea
 Specific symptoms
 Jaundice
 Purities
 Moderate pain
 DM
 Unexplained attack of pancreatitis
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43. Physical findings
 Jaundice
 Enlarged liver
 Courvoisier`s law
 Palpable mass)
 Ascites
 Virchow-Troisier node
 Sister Josephs node
 Wasting
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44.  LFT ( raised ALP, Bili.)
 CA 19-9
 CA 494
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45.  Ultrasound
 CT scan
 MRI
 Cholangiography
 E.R.C.P.
 P.T.C.
 M.R.C.P.
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46. Palliation
 Jaundice ( pruritis)
 Pain
 Duodenal obstruction
Curative
 Resection of the tumor (Whipple procedure /
Pancreaticoduodenectomy )
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49. 1) Pseudocyst (75-80%)
2) Common cystic pancreatic neoplasms
 Mucinous cystic neoplasm (10-45%)
 Serous cystic neoplasm (32-39%)
 IPMN (21-33%)
3) Rare cystic pancreatic neoplasms
 Solid pseudopapillary tumor (<10%)
 Acinar cell cystadenocarcinoma (<1%)
 Lymphangioma
 Hemangioma
 Paraganglioma

50. 4) Solid pancreatic lesions with cystic degeneration
 Pancreatic adenocarcinoma (<1%)
 Cystic islet cell tumor (insulinoma, glucagonoma,
gastrinoma) (<10%)
 Metastasis
 Cystic teratoma
 Sarcoma
5) Hydatid cyst
6) Lymphatic cyst
7) True epithelial cysts, associated with:
 von Hippel–Lindau disease
 Autosomal-dominant polycystic kidney disease

51.  Symptoms
 Abdominal pain (80 – 90%)
 Lump in abdomen
 Nausea / vomiting ( due to gastric or duodenal
compression)
 Early satiety
 Bloating, indigestion
 Jaundice ( due to compression of bile duct)
 Hemorrhage
 Signs
 Tenderness
 Abdominal fullness
 Palpable mass
 Blood test: amylase, lipase

52.  Ultrasonography
 Most practical & Sensitivity 75 – 90%
 limited by patient habitus, operator experience and air in stomach
 CT scan
 Gold standard for initial assessment and follow-up
 Sensitivity  90- 100%
 MRI
 Better detail of content of cyst
 MRCP
 Establish the relationship of the pseudocyst to the pancreatic ducts
 Endoscopic Ultrasonography (EUS +/- FNA)
 Distinguishing pancreatic cystic lesions, helps in FNA

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54.  Most common, 10% to 45%
 > 95% in women
 Mean age 50 years
 Typically involve the body and tail of the
pancreas
 Never multifocal, occurring only in one
location within the pancreas.

55.  Asymptomatic in 75% cases
 If symptoms, usually due to mass effect
 Addominal pain
 Palpable mass

56.  CT or MRI of the abdomen
 Complex macrocystic mass with internal septations
 MRCP no communication between duct and the cyst
 Presence of mural nodule and septal calcification
suspicion of malignancy

57.  Complex macrocystic lesion with internal septations
 Peripheral and septal calcification indicative of malignancy
(arrowheads)

58.  Second MC Cystic tumor of the pancreas
 Occurring mostly in women (75%) with a mean
62 years
 Most (50% to 70%) occur in the body or tail of the
pancreas
 An association with von Hippel-Lindau disease

59.  Mostly asymptomatic
 being detected during evaluation for other unrelated
conditions
 Can present with a palpable mass - size (10 to
25 cm)

60. Lesion with numerous
microcysts giving a
“honey-comb”
appearance
Lobulated outline
Central stellate scar

61.  Pathognomonic image by CT scan is that of a
spongy mass with a central “sunburst”
calcification - only 10% of patients
 location in the pancreatic body and tail
 wall thickness < 2 mm
 lobulated contour
 lack of communication with the pancreatic duct
 minimal wall enhancement

62.  Types - depend on involvement of duct
 main pancreatic duct, isolated side branches, or a combination of
both
 Benign (adenoma), borderline, or malignant
 Malignant neoplasms account for 60% of IPMNs

63.  Equal frequency in men and women
 Median age at diagnosis - about 65 years
 75% of patients are symptomatic
 Abdominal pain and weight loss – MC complaints
 Recurrent pancreatitis or
 Acute pancreatitis
 Patients with malignant neoplasms are more likely to be
 older and more likely to present with jaundice or new-onset
diabetes

64.  Differentiation of IPMN from other cystic
pancreatic masses may be difficult at CT
 Most reliable findings for the diagnosis
 Presence of a communication between the cystic lesion
and the main pancreatic duct
 Presence of mural nodules projecting into the
main pancreatic duct or cystic lesions

65.  Pathognomonic for IPMN in ERCP
 A wide and gaping papilla with secretion of mucin and filling
defects in the dilated pancreatic duct –FISH MOUTH
AMPULLA

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