pancreas for MBBS, undergraduate sudents

1. DR. PRAJWAL R K
DEPARTMENT OF GENERAL SURGERY
KEMPEGOWDA INSTITUTE OF MEDICAL SCIENCES, BANGALORE

2. • PANCREAS – GREEK ‘PAN’ (ALL) AND ‘KREAS’ (FLESH)
• DIVIDED INTO HEAD(30%), BODY AND TAIL(70%).
• 80–90% IS COMPOSED OF EXOCRINE ACINAR TISSUE
• WEIGHT – APPROXIMATELY 80 GRAMS

4. • THE HEAD LIES WITHIN THE
CURVE OF THE DUODENUM
• THE BODY OF THE SECOND
LUMBAR VERTEBRA AND THE
VENA CAVA.
• THE AORTA AND THE
SUPERIOR MESENTERIC
VESSELS LIE BEHIND THE
NECK OF THE GLAND.

5. • COMING OFF THE SIDE OF
THE PANCREATIC HEAD IS
THE UNCINATE PROCESS
• WHICH LIES BEHIND THE
SUPERIOR MESENTERIC VEIN.
• THE TIP OF THE PANCREATIC
TAIL EXTENDS UP TO THE
SPLENIC HILUM.

7. • 80–90% OF PANCREAS (EXOCRINE ACINAR TISSUE)
• ORGANIZED INTO LOBULES
• THE MAIN PANCREATIC DUCT BRANCHES INTO
INTERLOBULAR AND INTRALOBULAR DUCTS, DUCTULES AND,
FINALLY, ACINI.
• THE MAIN DUCT IS LINED BY COLUMNAR EPITHELIUM,
CUBOIDAL IN THE DUCTULES.

9. • CLUSTERS OF ENDOCRINE CELLS, KNOWN AS ISLETS OF
LANGERHANS
• 75% ARE B CELLS (PRODUCING INSULIN);
• 20% ARE A CELLS (PRODUCING GLUCAGON);
• D CELLS (PRODUCING SOMATOSTATIN)
• F CELLS (PANCREATIC POLYPEPTIDE)
• B CELLS FORM AN INNER CORE
• THE ISLET CELLS SPLENIC DRAIN INTO THE PORTAL VEIN

11. • DAY 26 – DORSAL
PANCREATIC DUCT ARISES
FROM THE DORSAL SIDE OF
THE DUODENUM
• DAY 32 – VENTRAL BUD
ARISES FROM THE BASE OF
THE HEPATIC DIVERTICULUM

12. • DAY 37 - CONTACT
OCCURS BETWEEN THE TWO
BUDS. FUSION BY THE END
OF WEEK 6

13. WEEK 6
• VENTRAL BUD PRODUCES THE HEAD
AND UNCINATE PROCESS
• DUCTS FUSE
• VENTRAL DUCT AND DISTAL PORTION
OF THE DORSAL DUCT FORM THE
MAIN DUCT (DUCT OF WIRSUNG)
• PROXIMAL DORSAL DUCT FORMS THE
DUCT OF SANTORINI

14. • MONTH 3 – ACINI APPEAR
• MONTHS 3–4 – ISLETS OF LANGERHANS APPEAR AND
BECOME BIOLOGICALLY ACTIVE

17. • ANTERIOR AND POSTERIOR SUPERIOR
PANCREATODUODENAL ARTERY BRANCH OF
GASTRO DUODENAL ARTERY
• ANTERIOR AND POSTERIOR INFERIOR
PANCREATODUODENAL ARTERY BRANCH OF
SUPERIOR MESENTERIC ARTERY.
• INFERIOR PANCREATIC ARTERY
• SUPERIOR PANCREATIC ARTERY
• SPLENIC AND LEFT GASTROEPIPLOIC ARTERY

21.  DUCT OF WIRSUNG (MPD) – EMPTIES INTO THE
AMPULLA OF VATER TOGETHER WITH THE CBD.
 DUCT OF SANTORINI – DRAINS INTO THE MINOR
PAPILLA APPROXIMATELY 2 CM ABOVE AND MEDIAL
TO THE AMPULLA OF VATER (MINOR DUCTAL
SYSTEM)

23. • ‘NORMAL’ PANCREATIC DUCTS
• 60%

24. SUPPRESSION OF THE ACCESSORY DUCT
(SANTORINI) – 30%
ACCESSORY DUCT DOES NOT OPEN
INTO THE MINOR DUODENAL PAPILLA
ACCESSORY DUCT DOES NOT
COMMUNICATE WITH THE MAIN
PANCREATIC DUCT

25. SUPPRESSION OF THE ACCESSORY DUCT
(SANTORINI) – 30%
ACCESSORY DUCT ABSENT

26. SUPPRESSION OF THE MAIN DUCT
(WIRSUNG) – 10%
ACCESSORY DUCT DOES NOT
COMMUNICATE WITH THE MAIN
PANCREATIC DUCT
OPEN SEPARATELY INTO THE
DUODENUM AT MAJOR AND MINOR
DUODENAL PAPILLA- THIS LEADS TO
PANCREAS DIVISUM

27. SUPPRESSION OF THE MAIN DUCT
(WIRSUNG) – 10%
MAIN PANCREATIC DUCT DUCT ABSENT

28. • THE OUTLET OF EACH DUCT IS PROTECTED BY
A COMPLEX SPHINCTER MECHANISM
1) SUPERIOR CHOLEDOCHAL
SPHINCTER
2) INFERIOR CHOLEDOCHAL
SPHINCTER
3) AMPULLARY SPHINCTER
4) PANCREATIC SPHINCTER

29. THERE IS A COMMON
CHANNEL WITH NO
SPHINCTER MECHANISM
PROTECTING FLOW
BETWEEN THE DUCTS
Gallstone pancreatitis is more likely

30. THERE IS A PARTIAL
COMMON CHANNEL
Gallstone pancreatitis is more likely

31. THERE IS SEPARATION OF
THE TWO CHANNELS

32.  APLASIA
 HYPOPLASIA
 HYPERPLASIA
 HYPERTROPHY
 DYSPLASIA
 ECTOPIC PANCREATIC TISSUE
 ACCESSORY PANCREAS
 VASCULAR ANOMALIES
 CHOLEDOCHAL CYSTS
 HORSESHOE PANCREAS
 VARIATIONS AND ANOMALIES OF
THE DUCTS
 PANCREAS DIVISUM
 ROTATIONAL ANOMALIES
 ANNULAR PANCREAS
 PANCREATIC GALL BLADDER
 POLYCYSTIC DISEASE
 CONGENITAL PANCREATIC CYSTS
 CYSTIC FIBROSIS
 VON HIPPEL–LINDAU
SYNDROME

33. ANNULAR PANCREAS
FAILURE OF COMPLETE ROTATION OF THE VENTRAL
PANCREATIC BUD
A RING OF PANCREATIC TISSUE SURROUNDS THE SECOND OR
THIRD PART OF THE DUODENUM.
ASSOCIATED WITH CONGENITAL DUODENAL STENOSIS OR
ATRESIA
MOST COMMONLY SEEN IN DOWN’S SYNDROME.
PRESENTS WITH DUODENAL OBSTRUCTION
TREATMENT IS BYPASS (DUODENODUODENOSTOMY).

35. PANCREAS DIVISUM
• MOST COMMON CONGENITAL PANCREATIC DUCTAL
ANATOMICAL VARIANT
• DOMINANT DORSAL DUCT WHICH DRAINS THROUGH THE
MINOR PAPILLA
• FAILURE OF FUSION OF DORSAL AND VENTRAL
PANCREATIC DUCT

36. • CLASSIC PANCREATIC DIVISUM ANATOMY
• SMALL VENTRAL DUCT DRAINS THROUGH MAJOR
PAPILLA
• LARGE DORSAL DUCT DRAINING THROUGH THE MINOR
PAPILLA
• NO COMMUNICATION BETWEEN THE VENTRAL AND
DORSAL DUCTS

38. CLINICAL FEATURES:
ASYMPTOMATIC
4-14% DETECTED AT AUTOPSY SERIES
3-8% AT ERCP
9% AT MRCP
RECURRENT ACUTE PANCREATITIS, CHRONIC PANCREATITIS
MINOR PAPILLA - INCOMPLETE DRAINAGE.
ONE OF THE CONGENITAL CAUSES FOR RECURRENT PANCREATITIS
IMAGING:
MRCP
EUS
ERCP

39. MRCP: (a) gall bladder, (b) bile duct crossing the (c) long duct of Santorini, (d) a
short pancreatic duct together with the bile duct on the major duodenal papilla,
(e) imaged with renal collecting system

40. TREATMENT:
ENDOSCOPIC SPHINCTEROTOMY AND STENTING
OF THE MINOR PAPILLA MAY RELIEVE THE
SYMPTOMS.
SURGICAL INTERVENTION
SPHINCTEROPLASTY,
PANCREATOJEJUNOSTOMY
RESECTION OF THE PANCREATIC HEAD.

41. 2 MAJOR FUNCTIONS – EXOCRINE AND ENDOCRINE
EXOCRINE PANCREAS
• THE PANCREAS SECRETES APPROXIMATELY 500 TO 800
ML PER DAY
• COLORLESS, ODORLESS, ALKALINE (PH-8.4), ISOSMOTIC
PANCREATIC JUICE.
• PANCREATIC JUICE IS A COMBINATION OF ACINAR CELL
AND DUCT CELL SECRETIONS.

43. • THE PROTEOLYTIC ENZYMES ARE SECRETED AS
PROENZYMES THAT REQUIRE ACTIVATION.
• TRYPSINOGEN ACTIVATION WITHIN THE PANCREAS IS
PREVENTED BY THE PRESENCE OF INHIBITORS THAT ARE
ALSO SECRETED BY THE ACINAR CELLS.
• A FAILURE TO EXPRESS A NORMAL TRYPSINOGEN
INHIBITOR, PANCREATIC SECRETORY TRYPSIN INHIBITOR
(PSTI),
• ALSO KNOWN AS SERINE PROTEASE INHIBITOR KAZAL
TYPE 1 (SPINK1),
• IS A CAUSE OF FAMILIAL PANCREATITIS

45. • THE PRESENCE OF PEPTIDES AND
FATTY ACIDS FROM FOOD TRIGGERS
THE RELEASE OF CHOLECYSTOKININ
(CCK).
• CCK INDUCES THE RELEASE OF
PANCREATIC ENZYMES INTO THE
DUODENAL LUMEN.
• S CELLS LOCATED IN THE
DUODENUM RELEASE SECRETIN IN
RESPONSE TO THE ACIDIFICATION OF
THE DUODENUM.
• SECRETIN INDUCES THE SECRETION
OF HCO3 − FROM PANCREATIC
CELLS INTO THE DUODENUM.

46. ENDOCRINE PANCREAS

47. SERUM ENZYME LEVELS
PANCREATIC FUNCTION TESTS
MORPHOLOGY
ULTRASOUND SCAN
COMPUTED TOMOGRAPHY
MAGNETIC RESONANCE IMAGING
ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY
ENDOSCOPIC ULTRASOUND
PLAIN RADIOGRAPHY
CHEST
UPPER ABDOMEN

48. • MEASUREMENT OF SERUM AMYLASE LEVELS CAN IDENTIFY
PANCREATIC PATHOLOGY AS SERUM AMYLASE RAISES IN
CONDITIONS LIKE ACUTE PANCREATITIS.
• THE SERUM AMYLASE RISES WITHIN A FEW HOURS OF
PANCREATIC DAMAGE AND DECLINES OVER THE NEXT 4-8
DAYS
SENSITIVE BUT NOT SPECIFIC

49. ■ UPPER GASTROINTESTINAL TRACT PERFORATION
■ MESENTERIC INFARCTION
■ TORSION OF AN INTRA-ABDOMINAL VISCUS
■ RETROPERITONEAL HAEMATOMA
■ ECTOPIC PREGNANCY
■ MACROAMYLASAEMIA
■ RENAL FAILURE
■ SALIVARY GLAND INFLAMMATION

50. • URINE AMYLASE
• AMYLASE : CREATININE RATIO
• SERUM LIPASE- MORE SPECIFIC THAN SERUM AMYLASE,
RAISES EARLY AND LASTS FOR LONG
PANCRETIC FUNCTION TESTS
LUNDH TEST- ORAL MEAL INGESTION
IV SECRETIN TEST
NBT PABA TEST
STOOL ELASTASE
Duodenal intubation and
measurement of amount
of secretion

51. • PANCREATIC EXOCRINE FUNCTION CAN BE ASSESSED BY DIRECTLY
MEASURING PANCREATIC SECRETION IN RESPONSE TO A
STANDARDISED STIMULUS – FOLLOWED BY DUODENAL INTUBATION
AND MEASUREMENT OF AMOUNT OF SECRETION
• THE STIMULUS TO SECRETION CAN BE
• A) PHYSIOLOGICAL, E.G. INGESTION OF A TEST MEAL, AS IN THE LUNDH
TEST
• B) PHARMACOLOGICAL, E.G. INTRAVENOUS INJECTION OF A HORMONE,
SUCH AS SECRETIN OR CCK.

52. NBT PABA TEST--
NITROBLUE TETRAZOLIUM–PARA-AMINOBENZOIC ACID
(NBT–PABA)
INDIRECT MEASURE OF PANCREATIC FUNCTION
NBT–PABA IS ADMINISTERED ORALLY AND DEGRADED BY
PANCREATIC ENZYME, AND THE BREAKDOWN PRODUCT
(PABA) IS ABSORBED AND EXCRETED IN THE URINE
URINARY PABA LEVELS IS MEASURED
PANCREOLAURYL TEST- SAME PRINCIPLE AS ABOVE-
FLUORESCEIN DILAURATE
URINARY FLUROSSCEIN LEVELS ESTIMATED
STOOL ELASTASE – ELASTASE LEVELS IN THE STOOL
IS MEASURED

53. • Abrupt cut off of colonic gas
coloumn at splenic flexure-
colon cutoff sign
• Colon beyond this point is
decompressed by normal
peristalsis

54. ULTRASONOGRAPHY IS THE INITIAL INVESTIGATION OF CHOICE IN PATIENTS WITH
JAUNDICE TO DETERMINE
 BILE DUCT IS DILATED OR NOT
 AND LIVER METASTASES PRESENT OR ABSENT
BULKY PANCREAS IN PANCREATITIS
VESSEL THROMBOSIS CAN BE IDENTIFIED
CAN DETECT MASS IN THE PANCREAS
PSEUDOCYST CAN BE IDENTIFIED EASILY
OBESITY AND OVERLYING BOWEL GAS ARE LIMITING FACTORS

56. PANCREATIC CARCINOMAS OF 1–2 CM IN SIZE CAN BE
IDENTIFIED
ENDOCRINE TUMOURS ARE ALSO WELL IMAGED
IN PANCREATITIS, NECROTIC AREAS WITHIN THE GLAND CAN BE
IDENTIFIED BY THE ABSENCE OF CONTRAST ENHANCEMENT ON
CT.
INFLAMMATORY COLLECTIONS AND PSEUDOCYSTS CAN BE SEEN

57. CT-GUIDED DRAINAGE IS HELPFUL IN THE TREATMENT OF
PANCREATIC COLLECTIONS, CYSTS AND PSEUDOCYSTS
FACILITATES PERCUTANEOUS FINE-NEEDLE OR TRUCUT
BIOPSY
PLUS IT IS NOT OPERATOR DEPENDENT AND BOWEL GAS
DOESN’T AFFECT IMAGING
CURRENT GOLD STANDARD FOR IMAGING PANCREAS

58. THE DILATED BILE DUCT (1) AND MAIN PANCREATIC DUCT (2) CAN BE SEEN, WITH TUMOUR
INFILTRATION AROUND THEM. THERE IS A THROMBUS IN THE SUPERIOR MESENTERIC VEIN (3).
THE GALL BLADDER IS DISTENDED (4)  CARCINOMA OF PANCREATIC HEAD

59. PANCREAS CAN BE CLEARLY IDENTIFIED, AND CLEAR IMAGES OF THE
BILE DUCT AND THE PANCREATIC DUCT, TOGETHER WITH FLUID
COLLECTIONS, CAN BE DEFINED.
SMALL TUMORS CAN BE IDENTIFIED IN THE HEAD/BODY OF
PANCREAS WITH GREATER ACCURACY THAN CT.
OTHER STRUCTURES LIKE BILE DUCTS AND PANCREATIC DUCTS CAN
ALSO BE IDENTIFIED.

61. MAGNETIC RESONANCE CHOLANGIOGRAPHY AND
PANCREATOGRAPHY (MRCP) IS A SPECIAL SEQUENCE OF MRI
MRCP IDENTIFIES BILE DUCTS AND OBSTRUCTION BETER THAN
OTHER MODALITIES AND GIVES INFORMATION SIMILAR TO ERCP
WITHOUT INVASIVE PROCEDURES
NO CONTRAST IS NEEDED

62. • USING MRCP IN CONJUNCTION WITH INTRAVENOUS
INJECTION OF SECRETIN, EMPTYING OF THE PANCREATIC DUCT
CAN BE DEMONSTRATED TO SHOW THE ABSENCE OR PRESENCE
OF OBSTRUCTION.

64. BOTH A DIAGNOSTIC AND THERAPEUTIC MODALITY
USING A SIDE-VIEWING ENDOSCOPE THE AMPULLA OF VATER
CAN BE IDENTIFIED AND CANNULATED
INJECTION OF WATER-SOLUBLE CONTRAST DIRECTLY INTO
THE BILE DUCT PROVIDES EXCELLENT IMAGES OF THE DUCTAL
ANATOMY

65. REDUCED USE FOR DIAGNOSTIC PURPOSES NOW –
ENDOSCOPIC ULTRASOUND AND MRCP
WIDESPREAD AVAILABILITY
CHEAPER
NON INVASIVE AND LESS RISKY
CURRENTLY MAINLY THERAPEUTIC
ERCP STILL HAS A REAL ROLE IN THE ASSESSMENT OF THE
PATIENT WITH OBSTRUCTIVE JAUNDICE.

67. IRREGULAR STRICTURE OF PACREATIC DUCT- S/O Carcinoma

68. • AN ULTRASOUND PROBE IS ATTACHED TO THE TIP OF ENDOSCOPE
AND VISUALIZATION OF DIFF LAYERS OF THE DUODENUM AND
PANCREAS IS POSSIBLE
• CAN ASSES:
• THE LOCATION AND DEPTH OF INVASION OF A TUMOUR
IN PANCREAS
• CALCULI IN PANCREATIC DUCT
• BIOPSY CAN ALSO BE TAKEN UNDER GUIDANCE
• ENDOSCOPIC DRAINAGE OF PSEUDOCYST

70. ‘PANCREATITIS IS INFLAMMATION OF THE PANCREATIC
PARENCHYMA’
• ACUTE PANCREATITIS
• RECURRENT PANCREATITIS
• CHRONIC PANCREATITIS

71. ACUTE PANCREATITIS IS DEFINED AS AN ACUTE
CONDITION PRESENTING WITH
• ABDOMINAL PAIN,
• A THREEFOLD OR GREATER RISE IN THE SERUM LEVELS OF THE
PANCREATIC ENZYMES AMYLASE OR LIPASE, AND/OR
• CHARACTERISTIC FINDINGS OF PANCREATIC INFLAMMATION
ON CONTRAST-ENHANCED CT

72. UNDER NORMAL CIRCUMSTANCES –
• PANCREAS PROTECTED FROM AUTO-DIGESTION BY FOLLOWING
MECHANISMS:
1. MOST DIGESTIVE ENZYMES ARE SYNTHESIZED AS
INACTIVE PRO ENZYMES
2. MOST OF THESE PRO ENZYMES ARE ACTIVATED BY
TRYPSIN IN THE DUODENUM, INTRAPANCREATIC
ACTIVATION OF THE ENZYMES IS MINIMAL

73. 3. TYPSINOGEN GETS ACTIVATED IN THE
DUODENUM
4. ACINAR AND DUCTAL CELLS SECRETES TRYPSIN
INHIBITORS, WHICH LIMITS INTRAPANCREATIC
TRYPSIN ACTIVITY

74. MILD (INTERSTITIAL OEDEMATOUS PANCREATITIS)
• INTERSTITIAL OEDEMA OF THE GLAND AND MINIMAL ORGAN
DYSFUNCTION.
• THE MAJORITY (80%) WILL HAVE MILD ATTACK OF PANCREATITIS,
• THE MORTALITY AROUND 1%
SEVERE (NECROTISING PANCREATITIS)
• SEEN IN 5–10% OF PATIENTS,
• PANCREATIC NECROSIS,
• A SEVERE SYSTEMIC INFLAMMATORY RESPONSE AND OFTEN MULTI-
ORGAN FAILURE.
• MORTALITY VARIES FROM 20 TO 50%.

75. • GALLSTONES (50-70%)
• ALCOHOLISM (20-25%)
• POST ERCP
• ABDOMINAL TRAUMA
• FOLLOWING BILIARY, UPPER GASTROINTESTINAL OR
CARDIOTHORACIC SURGERY
• AMPULLARY TUMOUR
• DRUGS (CORTICOSTEROIDS, AZATHIOPRINE, ASPARAGINASE,
VALPROIC ACID, THIAZIDES, OESTROGENS)

76. • HYPERPARATHYROIDISM
• HYPERCALCAEMIA
• PANCREAS DIVISUM
• AUTOIMMUNE PANCREATITIS
• HEREDITARY PANCREATITIS
• VIRAL INFECTIONS (MUMPS, COXSACKIE B)
• MALNUTRITION
• SCORPION BITE
• IDIOPATHIC

77. COMMON CHANNEL THEORY
• STONE LODGED AT AMPULLA OF VATER RESULTS IN
BILE REFLUX INTO PANCREATIC DUCT.
• AFTER PASSAGE OF GALL STONE THROUGH
SPHINCTER OF ODDI, IT BECOMES INCOMPETENT
AND RESULTS IN REFLUX OF DUODENAL FLUID AND
BILE INTO PANCREATIC DUCT.

78. GALL STONE BLOCKING PANCREATIC DUCT
DUCTAL HYPERTENSION
INCREASE BACK PRESSURE IN PANCREATIC DUCT
LEADS TO MINOR DUCTAL DISRUPTION
EXTRAVASATION OF PANCREATIC SECRETIONS INTO PARENCHYMA
PREMATURE ENZYME ACTIVATION

79. • EXCESSIVE ALCOHOL CONSUMPTION 100-150
GM/DAY;
• ETHANOL CONTENT IN ALCOHOL IS TOXIC TO
ACINAR CELLS CAUSING INCREASED SECRETION
FOLLOWED BY INHIBITION.
• ETHANOL CAUSES SPASM OF SPHINCTER OF ODDI.

80. • ETHANOL INDUCED INCREASED DUCT PERMEABILITY
ALLOWS PREMATURE ACTIVATION OF ENZYMES
CAUSING DAMAGE TO PANCREATIC PARENCHYMA.
• ETHANOL INCREASES PROTEIN CONTENT OF THE
PANCREATIC JUICE AND PROTEIN PLUG FORMATION
IN THE PANCREATIC DUCT CAUSING OBSTRUCTION.

81. ONCE CELLULAR INJURY HAS BEEN INITIATED THE
INFLAMMATORY PROCESS CAN LEAD TO-
• PANCREATIC EDEMA
• PANCREATIC HAEMORRHAGE
• PANCREATIC NECROSIS

82. AS INFLAMMATORY MEDIATORS ARE RELEASED INTO
CIRCULATION, SYSTEMIC COMPLICATIONS CAN OCCUR
• HEMODYNAMIC INSTABILITY
• BACTEREMIA
• ARDS
• PLEURAL EFFUSION
• GASTROINTESTINAL HEMORRHAGE
• RENAL FAILURE
• DIC

85. • NORMALLY PRO-ENZYMES WHICH ARE INACTIVE IN
PANCREAS TURNS INTO ACTIVE FORM IN THE
DUODENUM.
• TRYPSINOGEN CONVERTED TO TRYPSIN IN THE
DUODENUM.
• TRYPSIN CONVERTS OTHER PRO-ENZYMES INTO
ACTIVE FORM.

86. SIRS
Pancreatitis

88. INSULT
Sustained Rise in Ca2+
ZYMOGEN
GRANULES
Trypsinogen
LYSOSYMES
cathepsin B
Colocalization
Cathepsin B
↓
Trypsinogen → TRYPSIN
Colocalization
Cathepsin B
↓
Trypsinogen → TRYPSIN
Acinar cell death

89. SUSTAINED RISE IN CA2+
LYSOSOMAL (L) AND ZYMOGEN (Z) CONTENTS COLOCALIZE
TRYPSINOGEN IS ACTIVATED TO TRYPSIN BY CATHEPSIN B
TRYPSIN ↑ PERMEABILITY
CATHEPSIN B RELEASED IN TO CYTOSOL
CYTOCHROME C RELEASED FROM THE MITOCHONDRIA
APOPTOSIS

90. INSULT
↑ Ca2+
NF–KB
activation
PKC activation
Release of Cytokines and Chemokines
SYSTEMIC INFLAMMATION
SIRS → MODS → DEATH

91. PROTEIN KINASE C ENZYME
NUCLEAR FACTOR KAPPA AND BETA(NFKB)
RELEASE OF CYTOKINES AND CHEMOKINES
SYSTEMIC INFLAMMATORY RESPONSE (SIRS)
MODS
DEATH

92. TRYPSIN ACTS
AND STIMULATES
LIPASE
ACTS ON FAT
FATTY ACID
+GLYCEROL
FATTY ACIDS
+CALCIUM
CALCIUM SOAP
FAT NECROSIS
ELASTASE
DIGESTS ELASTIC
FIBERS OF BLOOD
VESSELS
PSEUDOANEURYS
M
RUPTURE
HAEMORRHAGE
DEATH
LYSOLECITHINASE
MEMBRANE
DAMAGE
NECROSIS
SPREADING
NECROTISING
PANCREATITIS
INFECTED
NECROSIS
PHOSPHOLIPASE
A2
PROSTAGLANDINS,
BRADYKININS
DIFFUSE
INFLAMMATION
ACUTE
HYPOVOLEMIC
SHOCK
RENAL FAILURE

93. SYMPTOMS:
EPIGASTRIC PAIN, SUDDEN ONSET, RADIATING TO
THE BACK (50%) WITH NAUSEA AND VOMITING.
PAIN IS FREQUENTLY SEVERE, CONSTANT AND
REFRACTORY TO THE USUAL DOSES OF ANALGESICS.
DISCOMFORT MAY BE RELIEVED BY SITTING OR
BENDING FORWARD AND AGGRAVATED BY LYING
DOWN.

94. SIGNS:
ABDOMINAL TENDERNESS.
ABDOMINAL DISTENSION (D/T ILEUS)
GUARDING IN UPPER ABDOMEN
SEVERE PANCREATITIS MAY LEAD TO RETROPERITONEAL
HEMORRHAGE WHICH LEADS TO : 1 . HYPOVOLEMIA
2. HYPOTENSION
3. TACHYCARDIA

95. • SIRS IS DEFINED BY THE PRESENCE OF TWO OR
MORE OF THE FOLLOWING CRITERIA:
• HEART RATE >90/MIN,
• CORE TEMPERATURE <36O C OR >38O C,
• RESPIRATIONS >20/MIN OR PCO2 <32 MMHG, AND
• WHITE BLOOD CELL COUNT <4000 OR >12 000/MM3.

96. CULLEN’S SIGN
(PERIUMBILICAL ECCHYMOSIS)
GREY TURNER’S SIGN
(FLANK ECCHYMOSIS)

97. • ACUTE CHOLECYSTITIS
• PERFORATED DUODENAL ULCER
• ACUTE MYOCARDIAL INFARCTION
• PNEUMONIA OR PLEURITIC PAIN.

98. IT IS DONE BY VARIOUS SCORING SYSTEMS:
1. BISAP SCORING SYSTEM (BEDSIDE INDEX OF SEVERITY IN ACUTE
PANCREATITIS)
2. RANSONS SCORING SYSTEM
3. GLASGOW SCORING SYSTEM
4. APACHE I , APACHE II, APACHE III (ACUTE PHYSIOLOGIC
ASSESMENT AND CHRONIC HEALTH EVALUATION)
5. CT SEVERITY INDEX (CTSI)
6. BALTHAZAR GRADING SYSTEM (CT)

100. ATLANTA CLASSIFICATION OF ACUTE PANCREATITIS BE STRATIFIED
INTO 3 GROUPS:
MILD ACUTE PANCREATITIS:
• NO ORGAN FAILURE;
• NO LOCAL OR SYSTEMIC COMPLICATIONS.
MODERATELY SEVERE ACUTE PANCREATITIS:
• ORGAN FAILURE THAT RESOLVES WITHIN 48 HOURS (TRANSIENT ORGAN FAILURE);/
• LOCAL OR SYSTEMIC COMPLICATIONS WITHOUT PERSISTENT ORGAN FAILURE.
SEVERE ACUTE PANCREATITIS:
• PERSISTENT ORGAN FAILURE (>48 HOURS);
• SINGLE ORGAN FAILURE;
• MULTIPLE ORGAN FAILURE.

101. SERUM AMYLASE
SERUM LIPASE

103. URINARY
TRIPSINOGEN-2
Amylase Lipase
Positive 35 30 34
Negative 3 1 2
False Positive 1 5 2
False Negative 0 3 1

104. • X-RAY ABDOMEN- COLON CUT OFF SIGN
• ULTRASOUND – SWELLING OF THE PANCREAS
AND LOSS OF TISSUE PLANES.
• CT SCAN – OBLITERATION OF FAT STRANDS,
EDEMA, NECROTIC AREAS.

105. • Abrupt cut off of colonic gas
column at splenic flexure-
colon cutoff sign
• Colon beyond this point is
decompressed by normal
peristalsis

106. • IF THERE IS DIAGNOSTIC UNCERTAINITY.
• IN SEVERE ACUTE PANCREATITIS.
• PATIENT WITH ORGAN FAILURE, SIGNS OF SEPSIS OR
PROGRESSIVE CLINICAL DETERIORATION.
• WHEN LOCALIZED COMPLICATION IS SUSPECTED
SUCH AS FLUID COLLECTION, PSEUDOCYST OR
PSEUDO ANEURYSM.

108. CT GRADE PATHOLOGY POINTS
A NORMAL 0
B OEDEMATOUS 1
C MILD EXTRAHEPATIC COLLECTION 2
D SEVERE EXTRAHEPATIC COLLECTION 3
E EXTENSIVE/MULTIPLE EXTRAHEPATIC COLLECTION 4

109. Management of
pancreatitis
is
PANCREAS

110. P -
A -
N -
C -
R
E - -
A -
S -

111. ADMISSION TO HDU/ICU
ANALGESIA
AGGRESSIVE FLUID REHYDRATION
OXYGENATION
INVASIVE MONITORING OF VITAL SIGNS, CENTRAL VENOUS
PRESSURE, URINE OUTPUT, BLOOD GASES
FREQUENT MONITORING OF HAEMATOLOGICAL AND
BIOCHEMICAL PARAMETERS (INCLUDING LIVER AND RENAL
FUNCTION, CLOTTING, SERUM CALCIUM, BLOOD GLUCOSE)

112. NASOGASTRIC DRAINAGE
ANTIBIOTIC PROPHYLAXIS CAN BE CONSIDERED (IMIPENEM,
CEFUROXIME)
ERCP WITHIN 72 HOURS FOR SEVERE GALLSTONE PANCREATITIS OR
SIGNS OF CHOLANGITIS
SUPPORTIVE THERAPY FOR ORGAN FAILURE IF IT DEVELOPS
(INOTROPES, VENTILATORY SUPPORT, HAEMOFILTRATION, ETC.)
NUTRITIONAL SUPPORT

113. • IT IS ESSENTIAL TO ESTABLISH THE ETIOLOGY .
• INVESTIGATE THOROUGHLY BEFORE LABELLING IT
AS IDIOPATHIC.
• IF THE ETIOLOGY IS GALL
STONES,CHOLECYSTECTOMY IS DESIRABLE DURING
THE SAME ADMISSION.
• SURGICAL INTERVENTIONS IN ACUTE
PANCREATITIS IS RESERVERD FOR
COMPLICATIONS.

115. • CARDIOVASCULAR
• PULMONARY
• RENAL FAILURE
• HAEMATOLOGICAL
• METABOLIC

116. • GASTROINTESTINAL
• NEUROLOGICAL
• MISCELLANEOUS

117. • PANCREATITIS MAY INVOLVE ALL ORGAN SYSTEMS
• SHOULD BE MANAGED BY A MULTIDISCIPLINARY TEAM
• INOTROPIC SUPPORT FOR HAEMODYNAMIC INSTABILITY,
• HAEMOFILTRATION IN THE EVENT OF RENAL FAILURE,
• VENTILATORY SUPPORT FOR RESPIRATORY FAILURE
• CORRECTION OF COAGULOPATHIES (INCLUDING DIC)
• THERE IS NO ROLE FOR SURGERY DURING THE INITIAL
PERIOD OF RESUSCITATION AND STABILISATION

118. LOCAL COMPLICATIONS (USUALLY DEVELOP AFTER 1ST WEEK):
• ACUTE FLUID COLLECTION
• STERILE PANCREATIC NECROSIS
• INFECTED PANCREATIC NECROSIS
• PANCREATIC ABSCESS
• PSEUDOCYST
• PANCREATIC ASCITES
• PLEURAL EFFUSION
• PORTAL/SPLENIC VEIN THROMBOSIS
• PSEUDOANEURYSM

119. • OCCURS EARLY IN THE COURSE OF MILD PANCREATITIS
WITHOUT NECROSIS
• LOCATED ADJACENT TO THE PANCREAS
• NO ENCAPSULATING WALL AND IS CONFINED WITHIN
NORMAL FASCIAL PLANES
• THE FLUID IS STERILE
• NO INTERVENTION IS NECESSARY
• LARGE COLLECTION CAUSES SYMPTOMS OR PRESSURE
EFFECTS
• PERCUTANEOUSLY ASPIRATED UNDER ULTRASOUND OR CT
GUIDANCE.
• TRANSGASTRIC DRAINAGE UNDER EUS GUIDANCE

120. • ‘PANCREATIC NECROSIS’ REFERS TO A DIFFUSE OR FOCAL
AREA OF NON-VIABLE PARENCHYMA
• CECT – ABSENCE OF PARENCHYMAL ENHANCEMENT
PANCREATIC NECROSIS
LYSIS OF PERIPANCREATIC FAT
ACUTE NECROTIC COLLECTION (ANC)
WELL-DEFINED INFLAMMATORY CAPSULE
WALLED-OFF NECROSIS (WON)
4 weeks

121. • NECROTISING PANCREATITIS ARE STERILE
• DUE TO TRANSLOCATION OF GUT BACTERIA
• BECOME SUBSEQUENTLY INFECTED NECROSIS
• MORTALITY RATE – 50%
• STERILE NECROTIC MATERIAL SHOULD NOT BE DRAINED

123. • INFECTED PANCREATIC NECROSIS BE DRAINED
• EITHER CT OR USG GUIDED
• IF THE SEPSIS WORSENS → PANCREATIC NECROSECTOMY
• DEBRIDEMENT OF THE DEAD TISSUE AROUND THE
PANCREAS
• HIGH MORBIDITY AND MORTALITY
• EITHER OPEN OR LAPAROSCOPIC

124. • AFTER NECROSECTOMY FURTHER NECROTIC TISSUE MAY
FORM.
• THERE ARE SEVERAL POSSIBLE WAYS OF DEALING WITH
THIS
• CLOSED CONTINUOUS LAVAGE
• CLOSED DRAINAGE
• OPEN PACKING
• CLOSURE AND RELAPAROTOMY

125. TUBE DRAINS ARE LEFT IN AND
THE RAW AREA FLUSHED
(BEGER)
• CONTINUOUS
POSTOPERATIVE CLOSED
LAVAGE OF THE LESSER SAC
AS ADVISED BY BEGER.
• LAVAGE IS CARRIED OUT
THROUGH SEVERAL
DOUBLE-LUMEN AND
SINGLE-LUMEN CATHETERS.
• EACH TIME, 1 LITRE OF
SALINE IS INFUSED
THROUGH AND THEN
DRAINED OVER A PERIOD
OF HOURS, AND THE
PROCESS IS REPEATED.

126. CLOSED DRAINAGE
• THE INCISION IS CLOSED, BUT THE CAVITY IS PACKED
WITH GAUZE-FILLED PENROSE DRAINS AND CLOSED
SUCTION DRAINS.
• THE PENROSE DRAINS ARE BROUGHT OUT THROUGH
THE FLANK AND SLOWLY PULLED OUT AND REMOVED
AFTER 7 DAYS.

127. • THE INCISION IS LEFT OPEN
• CAVITY IS PACKED WITH THE INTENTION OF RETURNING
TO THE OPERATING ROOM AT REGULAR INTERVALS
• REPACKING UNTIL THERE IS A CLEAN GRANULATING
CAVITY.

128. CLOSURE AND RELAPAROTOMY
• THE INCISION IS CLOSED WITH DRAINS WITH THE
INTENTION OF PERFORMING A SERIES OF
• PLANNED RELAPAROTOMIES EVERY 48–72 HOURS UNTIL
THE
• RAW AREA GRANULATES (BRADLEY).

129. • IT’S THE COLLECTION OF ENZYME RICH FLUID IN
PERITONEAL CAVITY DUE TO PANCREATIC DUCT
DISRUPTION.
• PARACENTESIS REVEAL HIGH AMYLASE LEVEL.
• OCTREOTIDE IS USED TO SUPPRESS THE
PANCREATIC SECRETION.
• ERCP DONE TO FIND OUT ANY PANCREATIC
DUCT DISRUPTION AND PLACEMENT OF STENT.

130. • OCCURS FOLLOWING AN ATTACK OF
PANCREATITIS DUE TO BLEEDING FROM
PSEUDANEURYSM OR PSEUDOCYST.
• HAEMORRHAGE OCCURS INTO GIT.
• WHEN BLEEDING OCCURS INTO PANCREATIC
DUCT IT IS CALLED HAEMOSUCCUS
PANCREATICUS

131. • THIS CONDITION OCCURS DUE TO ENZYMATIC
DIGESTION OF BLOOD VESSELS IN VICINITY OF
PANCREAS.
• USUALLY SPLENIC OR GASTRODUODENAL
ARTERY INVOLVED.
• IT HAS HIGH MORTALITY
• CT ANGIOGRAPHY FOLLOWED BY
EMBOLIZATION.
• IF NOT POSSIBLE OPEN LAPAROTOMY AND
LIGATION OF PSEUDOANEURYSM OR BLEEDING
VESSELS IN THE CAVITY.

132. • COLLECTION OF AMYLASE RICH FLUID IN LESSER
SAC DUE TO PANCREATIC PATHOLOGY.
• IT IS CALLED PSEUDOCYST BECAUSE IT HAS NO
EPITHELIAL LINING.
• IF FLUID COLLECTION OCCURS WITHIN 4 WEEKS
OF AP ITS CALLED ACUTE FLUID COLLECTION.
• AFTER 4 WEEKS OF AP, FLUID COLLECTION IS
CALLED PSEUDOCYST.

134. • ACUTE PANCREATITIS
• PANCREATIC INJURY
• CHRONIC PANCREATITIS

135. • BETWEEN STOMACH AND TRANSVERSE
COLON
• BETWEEN STOMACH AND LIVER
• BEHIND OR BELOW THE TRANSVERSE
COLON.

136. • TYPE 1-OCCURS AFTER ACUTE PANCREATITIS WITH
NORMAL PANCRETIC DUCT ANATOMY. HERE
PSEUDOCYST WILL NOT HAVE COMMUNICATION
WITH PD.
• TYPE 2-OCCURS AFTER ACUTE PANCREATITIS WITH
DISEASED PD. HERE CYST COMMUNICATES WITH PD.
• TYPE 3-OCCURS IN CHRONIC PANCREATITIS. HERE
STRICTURE PD AND CYST COMMUNICATES WITH THE
PD.

137. • TENSE CYSTIC MASS IN THE EPIGASTRIC,
UMBLICAL REGION EXTENDING INTO LEFT
HYPOCHONDRIUM.
• MASS DOES NOT MOVE WITH RESPIRATION, IT
DOES NOT FALL FORWARD.
• TRANSMITTED PULSATION FROM AORTA CAN BE
FELT.
• BAID SIGN: IF RYLES TUBE IS PASSED IT CAN BE
FELT OVER THE SWELLING.

138. • ULTRASOUND
• CT
• ENDOSCOPIC USG (DIAGNOSTIC &
THERAPEUTIC)
• ERCP, MRCP –TO KNOW WHETHER CYST IS
COMMUNICATING WITH PD

139. • PSEUDOCYST SHUD BE DIFFERENTIATED FROM
CYSTIC NEOPLASM OF PANCREAS.
• ASPIRATE THE FLUID AND SEND FOR ANALYSIS
OF CEA,AMYLASE ESTIMATION AND CYTOLOGY.

140. • PSEUDOCYST RESOLVES SPONTANEOUSLY IN
MAJORITY OF CASES.
• PSEUDOCYST WITH THICK WALL > 6 CMS ,IF CYST
PRESENT FOR > 12 WEEKS AND IF IT IS DUE TO
CHRONIC PANCRETITIS THEY ARE LESS LIKELY TO
RESOLVE.

141. PROCESS OUTCOMES
INFECTION ABSCESS
SYSTEMIC SEPSIS
RUPTURE
-INTO THE GUT
-INTO THE PERITONEUM
GASTROINTESTINAL BLEEDING
INTERNAL FISTULA
PERITONITIS
ENLARGEMENT
-PRESSURE EFFECTS
-PAIN
OBSTRUCTIVE JAUNDICE FROM
BILIARY COMPRESSION
BOWEL OBSTRUCTION
EROSION INTO A VESSEL HAEMORRHAGE INTO THE CYST
HAEMOPERITONEUM

142. DRAINAGE OF PSEUDOCYST OF PANCREAS:
1. PERCUTANEOUS DRAINAGE
2. ENDOSCOPIC DRAINAGE
3. SURGICAL

143. PERCUTANEOUS DRAINAGE
• PERCUTANEOUS TRANS GASTRIC
CYSTOGASTROSTOMY IS DONE UNDER IMAGING
GUIDANCE.
• HERE DOUBLE PIGTAIL DRAIN,ONE END IN CYST
CAVITY AND OTHER END IN GASTRIC LUMEN.

144. ENDOSCOPIC DRAINAGE
• USUALLY INVOLVES
PUNCTURE OF CYST
THROUGH STOMACH
OR DUODENAL
WALL.
• UNDER EUS
GUIDANCE AND
PLACEMENT OF TUBE
DRAIN-ONE IN THE
CAVITY AND OTHER
IN THE LUMEN.

145. INTERNAL DRAINAGE OF PSEUDOCYST,
1. CYSTO-GASTROSTOMY
2. CYSTO-JEJUNOSTOMY

146. CYSTO-GASTROSTOMY

147. CYSTO-JEJUNOSTOMY

148. PROGRESSIVE INFLAMMATORY DISEASE WITH IRREVERSIBLE
DESTRUCTION OF PANCREATIC TISSUE.
CLINICAL COURSE
SEVERE PAIN
LATER STAGES, EXOCRINE AND ENDOCRINE PANCREATIC
INSUFFICIENCY
SOUTHERN INDIA, THE PREVALENCE IS MUCH HIGHER (100–200
PER 100 000).
MALE: FEMALE RATIO OF 4:1
MEAN AGE OF ONSET IS ABOUT 40 YEARS

149.  PANCREAS BECOMES SMALL, INDURATED AND
NODULAR AND EDGES BECOME ROUNDED.
 ALTERNATING AREAS OF STRICTURES AND DILATATIONS
IN THE DUCT WITH CALCIFICATIONS.
 MORE OF A CLINICAL DIAGNOSIS THAN
PATHOLOGICAL DIAGNOSIS

150. ETIOLOGY
GENETIC MUTATIONS,
ALCOHOL EXPOSURE,
DUCT OBSTRUCTION DUE TO TRAUMA, GALLSTONES, AND
TUMORS,
METABOLIC DISEASES SUCH AS HYPERLIPIDEMIA AND
HYPERPARATHYROIDISM,
AUTO-IMMUNE DISEASE.
TROPICAL PANCREATITIS

152. Toxic-Metabolic Idiopathic Genetic Autoimmune Recurrent
and
Severe
Acute
Obstructi
ve
•Alcoholic
•Tobacco
smoking
•Hypercalcemia
•Hyperlipidemi
a
•Chronic renal
failure
•Medications
•Toxins
•Early onset
•Late onset
•Tropical
(tropical
calcific and
fibrocalculous
•pancreatic
diabetes)
•Other
•Autosomal
dominant: cationic
trypsinogen gene –
(PRSS1 gene)
•Autosomal
recessive:
•CFTR
mutations,
•SPINK1
mutations,
cationic
trypsinogen
•α1-antitrypsin
deficiency
•Isolated
autoimmune
chronic
pancreatitis
•Syndromic
autoimmune
chronic
pancreatitis
Eg:Sjogren
syndrome–
associated
•Vascular
disease/
ischemic
•Radiation
injury
•Postnecroti
c
(severe
acute
pancreatitis)
•Pancreas
divisum
•Duct
obstructio
n
(e.g.,
tumor)
•Posttrau
matic
pancreati
c duct
scars

153. ALCOHOL (DRUNKARD’S PANCREAS)
60–70% OF CASES
HIGHEST IN HEAVY (>150 G/D) DRINKERS
PATHOLOGY IS UNCLEAR
REPEATED INFLAMMATION
GENETIC AND METABOLIC FACTORS MAY PLAY A ROLE

154. • FORM OF IDIOPATHIC PANCREATITIS
• BEGINS AT A YOUNG AGE
• HIGH INCIDENCE OF DIABETES MELLITUS AND STONE
FORMATION
• HIGH INCIDENCE IN KERALA.
• MECHANISMS FOR TROPICAL PANCREATITIS
• MALNUTRITION,
• INGESTION OF CYANOGENIC GLYCOSIDES IN CASSAVA ROOT,
• EXPOSURE TO HYDROCARBONS RELEASED BY KEROSENE OR
PARAFFIN LAMPS

155. TAPIOCA / CASSAVA/ SWEET POTATO

156. GENETIC FACTORS IN DEVOLOPMENT OF
CHRONIC PANCREATITIS
• PRSS-1 [PROTEASE SERINE -1]
• CHROMOSOME 7
• MUTATION OF CATIONIC TRYPSINOGEN GENE
• LEADS TO LOSS OF AUTOREGULATION OF TRYPSIN
• MUTANT TRYPSIN ACTIVATE OTHER PROENZYME AND
PRODUCE CLINICAL & SUBCLINICAL EPISODES OF AP
AND ULTIMATELY LEADS TO CHRONIC PANCREATITIS.

157. • SPINK-1[SERINE PROTEASE INHIBITOR KAZAL TYPE-1]
GENE MUTATION LEADS TO NON INHIBITION OF
TRYPSIN -- PRODUCING CLINICAL OR SUB CLINICAL
EPISODE OF ACUTE PANCREATITIS >> CHRONIC
PANCREATITIS.
• CFTR GENE – CYSTIC FIBROSIS TRASMEMBRANE
CONDUCTANCE REGULATOR GENE
• ALL THE ABOVE GENETIC FACTORS LEAD TO
DEVELOPMENT OF HEREDITARY (AD) AND IDIOPATHIC
PANCREATITIS

158. • AUTOIMMUNE PANCREATITIS MAY OCCUR IN ASSOCIATION WITH
OTHER AUTOIMMUNE DISEASES AS
• MULTIPLE SYSTEM DISORDER OR MAY AFFECT THE
PANCREAS ALONE EG: SJOGRENS SYNDROME, PRIMARY
BILIARY CIRRHOSIS, PRIMARY SCLEROSING CHOLANGITIS.
• AUTOANTIBODIES MAY BE PRESENT AND LEVEL OF THE
IMMUNOGLOBULIN SUB TYPE IGG4 ARE ELEVATED.

160. IN CHRONIC PANCREATITIS
REPEATED EPISODES OF
ACINAR CELL INJURY LEAD TO
PRO FIBROGENIC CYTOKINES
TRANSFORMING
GROWTH FACTOR –
BETA[TGF-B]
PLATELET-DERIVED
GROWTH
FACTOR[PDGF]
BOTH TGF-B AND PDGF
INDUCE ACTIVATION AND
PROLIFERATION OF
PANCREATIC STELLATE CELLS
RESULTING IN THE
DEPOSITION OF COLLAGEN
AND FIBROSIS

161. “Multiple hit” theory
of the etiology of
chronic
pancreatitis.
Multiple episodes of
acute pancreatitis
cause progressively
more organized
inflammatory
changes that
ultimately result
in chronic
inflammation and
scarring.

162. CLINICAL MANIFESTATIONS
1. HISTORY OF ALCOHOLISM AND RECURRENT ATTACKS OF
PANCREATITIS
2. PAIN-RADIATING TO BACK
3. DIABETES
4. STEATORRHEA.
5. FREQUENT ASSOCIATED WITH PSEUDOCYST.
6. ANOREXIA AND WEIGHT LOSS

163. PAIN LOCATION IN CHRONIC PANCREATITIS

165. STEATORRHEA
• IT IS THE PRESENCE OF EXCESS FAT IN FEACES.
STOOLS ARE BULKY AND DIFFICULT TO FLUSH.
• STEATORRHEA DOES NOT OCCUR UNTIL PANCREATIC
LIPASE SECRETION IS REDUCED TO LESS THAN 10%
OF MAXIMUM OUT PUT
• IT IS A FEATURE OF FAR ADVANCED PANCREATITIS

166. INVESTIGATIONS
 PANCREATIC FUNCTION TESTS- DECREASED FUNCTION AND
PANCREATIC INSUFFICIENCY
 XRAY ABDOMEN- PANCREATIC CALCIFICATIONS
 USG ABDOMEN- PANCREATIC CALCIFICATIONS, PSEUDOCYSTS
AND DECREASED GLAND SIZE

168. INVESTIGATIONS
 CT ABDOMEN- THE MAIN AREA OF DAMAGE AND THE
POSSIBILITIES FOR SURGICAL CORRECTION
 MRCP - WILL IDENTIFY THE PRESENCE OF BILIARY OBSTRUCTION
AND THE STATE OF THE PANCREATIC DUCT .
 ERCP- MOST ACCURATE WAY OF ELUCIDATING THE ANATOMY OF
THE DUCT AND, IN CONJUNCTION WITH THE WHOLE ORGAN
MORPHOLOGY, CAN HELP TO DETERMINE THE TYPE OF OPERATION
REQUIRED.

170. • NON INVASIVE
• ASSES PANCREATIC PARENCHYMA AND DUCTS AT THE
SAME TIME
• IT CAN DETCT PANCREATIC DUCTAL DILATATION, FILLING
DEFECTS AND NARROWING

171. DILATEDPANCREATICDUCTWITHCALCIFICATIONS

173. • PROVIDES MOST ACCURATE VISUALIZATION OF THE PANCREATIC
DUCTAL SYSTEM
• GOLD STANDARD FOR THE DIAGNOSIS OF CHRONIC PANCREATITIS
• FINDINGS INCLUDE
• CHAIN OF LAKES - BEADING OF THE MAIN PANCREATIC
DUCT
• INTRA DUCTAL FILLING DEFECTS

175. ERCP IN A PATIENT WITH
CHRONIC PANCREATITIS
SHOWS CALCIFICATIONS
IN THE REGION OF THE
PANCREATIC HEAD AND
CONCOMITANT DISTAL
COMMON BILE DUCT
STENOSIS.

176. PANCREATOGRAM SHOWS A DILATED AND
TORTUOUS PANCREATIC DUCT WITH MULTIPLE
SIDE BRANCHES.

178. • VISUALIZES BOTH THE PANCREATIC DUCTS AND THE
PARENCHYMA
• EUS HAS THE ABILITY TO DETECT CP IN PATIENTS WITH
EARLY STAGE
• EUS FEATURES OF CP INCLUDE DUCTAL AND
PARENCHYMAL CHANGES

179. Parenchymal abnormality
hyperechoic foci
hyperechoic strands
Lobularity of contour
Cysts
Ductal Abnormilities
Main duct dilatation
Main duct irregularity
Hyperechoic ductal wall
Visible side duct
calcification

184. CALCIFICATIONS OF CHRONIC
PANCREATITIS

185. CALCIFICATIONS OF CHRONIC
PANCREATITIS

186. MEDICAL MANAGEMENT
-TREAT THE ALCOHOL ADDICTION
-ALLEVIATE ABDOMINAL PAIN
ELIMINATE OBSTRUCTIVE FACTORS (DUODENUM,
BILE DUCT, PANCREATIC DUCT)
ESCALATE ANALGESIA IN A STEPWISE FASHION
FOR INTRACTABLE PAIN, CONSIDER CT/EUS-
GUIDED COELIAC AXIS BLOCK

187. MEDICAL MANAGEMENT
NUTRITIONAL AND DIGESTIVE MEASURES
DIET: LOW IN FAT AND HIGH IN PROTEIN AND CARBOHYDRATES
PANCREATIC ENZYME SUPPLEMENTATION WITH MEALS
CORRECT MALABSORPTION OF THE FAT-SOLUBLE VITAMINS (A, D,
E,K) AND VITAMIN B12
MEDIUM-CHAIN TRIGLYCERIDES IN PATIENTS WITH SEVERE FAT
MALABSORPTION (THEY ARE DIRECTLY ABSORBED BY THE SMALL
INTESTINE WITHOUT THE NEED FOR DIGESTION)
REDUCING GASTRIC SECRETIONS
TREAT DIABETES MELLITUS

188. • PAPILLARY STENOSIS: PANCREATIC DUCT SPHINCTEROTOMY WILL
FACILITATE DRAINAGE
• PANCREATIC DUCT STRICTURE: SPHINCTEROTOMY, DILATATION AND
STENT PLACEMENT
• PANCREATIC DUCT CALCULI: SPHINCTEROTOMY, DILATATION AND
STONE EXTRACTION WITH STENTING.

189. SURGICAL MANAGEMENT
1) DRAINAGE PROCEDURE
a) LATERAL PANCREATICOJEJUNOSTOMY (PUESTOW’S PROCEDURE)
b) LATERAL PANCREATICOJEJUNOSTOMY (PARTINGTON – ROCHELLE OPERATION– SPLEEN
IS PRESERVED)
2) RESECTIVE PROCEDURE
a) WHIPPLE’S PROCEDURE
b) DISTAL PANCREATECTOMY
c) TOTAL PANCREATECTOMY
d) PANCREATODUODENECTOMY OR A BEGER PROCEDURE (DUODENUM-PRESERVING
RESECTION OF THE PANCREATIC HEAD) – IF MASS IS THERE AT THE HEAD OF
PANCREAS
e) DECORING OF HEAD OF PANCREAS WITH PANCREATOJEJUNOSTOMY OR FREY
PROCEDURE- IF DUCT IS DILATED OR MULTIPLE CALCULI ARE PRESENT

190. Puestow’s procedure
• Lateral
Pancreaticojejunost
omy
• Tail of the pancreas
is removed along
with Spleen

191. Partington – Rochelle operation
Lateral Pancreatico jejunostomy
(Spleen is preserved)

192. Frey procedure
Decoring of head
of pancreas with
pancreatojejunosto
my

193. Beger procedure
(Duodenum-preserving
pancreatic head resection
(DPPHR))

194. PROGNOSIS
• THE OVERALL SURVIVAL RATE IS 70% AT 10
YEARS AND 45% AT 20 YEARS
• THE RISK OF DEVELOPING PANCREATIC
CANCER IS APPROXIMATELY 4% AT 20YEARS

195. CARCINOMA PANCREAS
EXOCRINE TUMORS
1. PANCREATIC DUCTAL
ADENOCARCINOMA
2. PANCREATOBLASTOMA
3. ACINAR CELL CARCINOMA
4. INTRADUCTAL PAPILLARY
MUCINOUS NEOPLASMS
5. MUCINOUS CYSTIC NEOPLASMS
6. SOLID-PSEUDOPAPILLARY
NEOPLASMS
ENDOCRINE TUMORS
1. INSULINOMA (Β CELLS) WHIPPLE’S
TRIAD
2. GASTRINOMA (G CELLS) PEPTIC
ULCER.
3. GLUCAGONOMA (Α CELLS) DIABETES,
NECROLYTIC MIGRATORY ERYTHEMA.
4. VIPOMA—PANCREATIC WATERY
DIARRHOEA, CHOLERA (VERNER-
HYPOKALAEMIA MORRISON
SYNDROME) ACHLORHYDRIA. (WDHA
SYNDROME)
5. SOMATOSTATINOMA. DIABETES, (S
CELLS) Δ CELLS STEATORRHOEA,
GALLSTONES.

196. D E M O G R A P H I C F A C T O R S
• AGE (PEAK INCIDENCE 65–75 YEARS)
• MALE GENDER
• BLACK ETHNICITY
E N V I R O N M E N T / L I F E S T Y L E – CIGARETTE SMOKING
G E N E T I C F A C T O R S A N D M E D I C A L C O N D I T I O N S
• FAMILY HISTORY
• TWO FIRST-DEGREE RELATIVES WITH PANCREAS CANCER: RELATIVE RISK INCREASES 18- TO 57-FOLD
• 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)
• LYNCH SYNDROME (HNPCC)
• 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

197. 1. CYSTADENOMA/CYSTADENOCARCINOMA:
SEROUS TYPE ( BENIGN)
A. RARE; PREDILECTION FOR FEMALES
B. CYSTIC SPACES DIVIDED BY FIBROUS SEPTA; VASCULAR
C. BETTER PROGNOSIS THAN ADENOCARCINOMA
D. TX. - RESECTION

198. MUCINOUS TYPE:
THEY INCLUDE :
• MUCINOUS CYSTIC NEOPLASMS (MCNS)
• INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMS(IPMNS).
MCNS ARE
 SEEN IN PERIMENOPAUSAL WOMEN,
 CONSISTS OF MULTILOCULAR THICK-WALLED CYSTS IN THE
PANCREATIC BODY OR TAIL
 HISTOLOGICALLY, CONTAIN AN OVARIAN TYPE STROMA.

199. INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMS
(IPMNS)
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 TENDENCYTO PROVE MALIGNANT

200. 2. ADENOCARCINOMA (DUCTAL)
A. 90% OF CASES; USUALLY AT THE HEAD.
B. PERIAMPULLARY MALIGNANCY
I. HEAD OF THE PANCREAS – 83%
II. AMPULLA OF VATER – 10%
III. DUODENUM – 4%
IV. COMMON BILE DUCT – 3%
C. SOLID, SCIRRHOUS TUMOURS, CHARACTERISED BY NEOPLASTIC
TUBULAR GLANDS WITHIN A MARKEDLY DESMOPLASTIC
FIBROUS STROMA.

201. WEIGHT LOSS – MOST COMMON
PAIN – DULL EPIGASTRIC PAIN THAT RADIATES
TO THE BACK; AGGRAVATED BY EATING AND
UPPER ABDOMINAL DISCOMFORT
PROGRESSIVE JAUNDICE – 75% SECONDARY
TO OBSTRUCTION OF THE DISTAL BILE DUCT IS
THE MOST COMMON SYMPTOM

202.  ANOREXIA AND WEAKNESS, NEW ONSET DIABETES
 PRURITUS, DARK URINE AND PALE STOOLS WITH STEATORRHOEA
OBSTRUCTIVE JAUNDICE.
 ENLARGED PALPABLE GALLBLADDER – COURVESIURE’S LAW
IN A JAUNDICED PATIENT- PALPABLE GALL-BLADDER IS
SELDOM DUE TO STONES

204. ALKALINE PO4
GGT
SGOT
SGPT
DIRECT BILIRUBIN
TOTAL BILIRUBIN
UROBILINOGEN
•

205. INVESTIGATIONS
• USG: INCREASED SIZE OF PANCREAS AND DILATED DUCTS WITH
OCCASIONAL FINDINGS OF WELL DEFINED MASS/ CYSTIC MASS
• ENDOSCOPY: CAN VISUALIZE GROWTH AT THE PERIAMPULLARY
REGION IN SECOND PART OF DUODENUM AND BIOPSY CAN ALSO BE
TAKEN .
• ENDOSCOPIC ULTRASOUND: CAN DEMONSRATE VASCULAR
INVASION AND CAN SEPERATE CYSTIC TUMOURS FROM PSEUDOCYSTS
TRANSDUODENAL OR TRANSGASTRIC FNA OR TRUCUT BIOPSY CAN
PERFORMED UNDER EUS GUIDANCE

206. PERIAMPULLARY GROWTH ON ENDOSCOPY

207. CARCINOMA
PANCREAS
ON EUS

208. INVESTIGATIONS
CECT ABDOMEN :
CAN ESTABLISH IF THERE IS A TUMOUR IN THE PANCREAS AND IF
IT IS RESECTABLE OR NOT.
PRESENCE OF HEPATIC OR PERITONEAL METASTASES OR LYMPH
NODE METASTASES DISTANT FROM THE PANCREATIC HEAD
ENCASEMENT OF THE SUPERIOR MESENTERIC, HEPATIC OR
COELIAC VESSELS
MRI AND MR VENOGRAPHY:
SIMILAR INFORMATION AS CT

210. IT IS INDICATED(ALONG WITH BILIARY STENTING)
WHEN
SUSPICION OF CHOLANGITIS
DIAGNOSTIC CONFIRMATION
RELIEVE JAUNDICE IF SURGERY IS DELAYED
PALLIATIVE STENTING IN INOPERABLE CASES

213. MANAGEMENT
ON PRESENTATION >85% TUMORS ARE NOT RESECTABLE.
RESECTBILITY IS ASSESED BY:
HEPATIC OR PERITONEAL METASTASES,
LYMPH NODE METASTASES DISTANT
FROM THE PANCREAS
ENCASEMENT OF THE MAJOR VESSELS
TUMOUR SIZE,
CONTINUOUS INVASION OF THE
DUODENUM, STOMACH OR COLON,
LYMPH NODE METASTASES WITHIN
THE OPERATIVE FIELD
NO RESECTION
NO CONTRA-
INDICATION

214. SURGICAL TREATMENT
WHIPPLES PROCEDURE:
IT INVOLVES REMOVAL OF TUMOR WITH
HEAD AND NECK OF PANCREAS, C LOOP OF DUODENUM,
DISTAL STOMACH, PROXIMAL JEJUNUM, LOWER END
OF THE COMMON BILE DUCT, GALLBLADDER AND INVOLVED LYMPH
NODES
IT CONSISTS OF 3 MAIN STEPS:
 CHOLEDOCHOJEJUNOSTOMY
 PANCREATICOJEJUNOSTOMY
 GASTROJEJUNOSTOMY

217. VS

218. ADEQUATE NUTRITIONAL PREPARATION OF THE PATIENT
PREOPERATIVELY
CLOSE POST OPERATIVE MONITORING
PARENTERAL NUTRITION POST OPERATIVELY
WATCH FOR COMPLICATIONS LIKE PANCREATIC FISTULA, LEAK OF THE
ANASTOMOTIC SITE ETC…
PREVENT POST OP COMPLICATIONS LIKE DVT , ATELECTASIS
FOLLOW UP WITH CHEMOTHERAPY AFTER SURGERY

220. • RELIEVE JAUNDICE AND TREAT BILIARY SEPSIS
SURGICAL BILIARY BYPASS
STENT PLACED AT ERCP OR PTBD
• IMPROVE GASTRIC EMPTYING
SURGICAL GASTROENTEROSTOMY
DUODENAL STENT
• PAIN RELIEF
STEPWISE ESCALATION OF ANALGESIA
COELIAC PLEXUS BLOCK

221. PERCUTANEOUS TRANS HEPATIC BILIARY DRAINAGE

222. • SYMPTOM RELIEF AND QUALITY OF LIFE
ENCOURAGE NORMAL ACTIVITIES
ENZYME REPLACEMENT FOR STEATORRHOEA
TREAT DIABETES
• 5-FU/GEMCITABINE BASED CHEMOTHERAPHY.
• EXTERNAL BEAM RADIATION- RARELY USED DUE TOXICITY OF
VITAL ORGANS AROUND THE PANCREAS.