This document provides information about pancreatitis, including: 1. It describes the anatomy, histology, and physiology of the pancreas. 2. It discusses acute pancreatitis in terms of causes, symptoms, investigations, severity scoring, and complications. Gallstones and alcohol are the most common causes. 3. It covers chronic pancreatitis, which is characterized by long-term inflammation, fibrosis, and loss of pancreatic function. Alcohol intake is the most common cause in adults. Symptoms include abdominal pain and malabsorption.

1. PANCREATITIS
Prepared by : Rita Imad Batta
supervised by: Dr. Abduljabar
Samara

2. Pancreas
 Anatomy, histology and physiology
 Acute pancreatitis
 Chronic pancreatitis

3. Pan
All Flesh
creas

5. Anatomy
 An accessory digestive gland
 Retroperitoneal
 Post to stomach, b/w duodenum and spleen
 Head, neck, body and tail
 Exocrine and endocrine
 Blood supply: splenic, gasroduodenal and SMA
 Venous drainage: pancreatic veins
 Innervation: parasympathetic from vagus.
Superior mesentric plexus
 Lymphatic drainage to celiac and SM lymph
nodes.

9. Blood supply

10. Venous drainage

11. Lymphatics

12. Innervation

14. Histology

15. MPD:
Wirsung
APD: Santorini

17. Physiology
 Endocrine: Insulin, Glucagon and somatostatin.
 Exocrine : basophilic cells and centriacinar cells
HCO3-rich alkaline fluid + enzymes to digest :
• Proteins: trypsin,chymotrypsin and
carboxypeptidase.
• Carbohydrate: amylase
• Fat: lipase, phospholipase and
cholesterolesterase.

18. Control over the pancreas
(Parasymathetic nerve endings): Enzymes
/pancreozymin: Enzymes
: HCO3
Both CCK and Secretin are secreted from
duodenum and jejunum
CCK: in response to chyme
Secretin: in response to highly acidic chyme

19. Proteolytic enzymes
 Inactive form: trypsinogen,
chymotrypsinogen and
procarboxypolypeptidase.
 Activated by trypsin
 Enterokinase ( when chyme contacts
intestinal mucosa)
 Smart pancreatic acinar cells secrete trypsin
inhibitor meanwhile !

20. Pancreatitis
Inflammation of the parenchyma of the pancreas
Pathophysiology
is premature activation of proteolytic enzymes
 AUTODIGESTION!
What cause premature activation of the
enzymes?
-Sever damage or injury to the pancreas
-Duct obstruction
Acute and chronic

21. Acute pancreatitis
 Incidence : 3% of all cases of abd. Pain
 Etiology:
1. Gallstones 60%
2. Alcoholism 25%
3. Idiopathic (no more
than 20%)
4. Post-ERCP 2%
5. Abd.Trauma 1.5%
6. Following a surgery
7. Ampullary tumor
8. Drugs
8. Hypercalcemia
9. Autoimmune
10. Toxins
11. Hereditary
12. Varial
13. Malnutrition
Bailey and Love’s

22. Causes of Acute Pancreatitis
 Biliary diseases
 Gallstones
 Choledocholithiasis
 Biliary sludge
 Microlithiasis
 Ethanol abuse
 Mechanical/structural injury
 Sphincter of Oddi dysfunction
 Pancreas divisum
 Trauma
 Postendoscopic retrograde
cholangiopancreatography
 Pancreatic malignancy
 PUD
 IBD
 Medications
 Azathioprine/6-mercaptopurine
 Dideoxyinosine
 Pentamidine
 Sulfonamides
 Thiazide diuretics
 ACEI
 Metabolic
 Hypertriglyceridemia
 Hypercalcemia
 Infectious
 Viral
 Bacterial
 Parasitic
 Vascular
 Vasculitis
 Genetic predisposition
 idiopathic
Doctor Qusay Abdoh

23. REMEMBER : “I GET SMASHED”!
 I : Idiopathic
 G : Gallstones
 E : Ethanol
 T :Trauma
 S : Scorpion bite (toxins)
 M : Mumps (Viral)
 A : Autoimmune
 S : Steroids
 H : Hyperlipidemia
 E : ERCP
 D : Drugs

24. 1. Gallstone pancreatitis
(50-70)%
 Triggered by the passage of gallstones down the
common bile duct  stones occlude the lumen
or cause back-flow  increase pancreatic duct
pressure  pooling of the enzymes 
autodigestion
 Increased risk :
1. wide cystic duct
2. small stones
3. common channel (MPD and CBD) prior to
ampulla ofVater.

27. 2. Alcohol 25%
 Habitual drinking over 5-15 years
 Usually causes acute exacerbation of chronic
pancreatitis BUT weekend binging habit or sole large
amount  precipitate a first attack
 Pathogenesis: multiple etiologies
• Direct toxic effect :
• intracellular accumulation and premature activation
• Increase the protein content and decrease the fluid
protein blug  duct obstruction
• Decrease trypsin inhibitor
• Also, malnutrition, dyslipidemia, hypersecretion
and concomitant tobacco smoking.

30. 3. Post-ERCP (1-3)%
 Pathogenesis is duct disruption and enzyme
extravasation.
 The risk is both endoscopist and patient
dependent (inexperienced endoscopist/
manometry is performed in the sphincter of
Oddi/ a patient with sphincter of Oddi
dysfunctiona)

32. 4. Abdominal trauma 1.5%
 Penetrating, blunt and cruch.
 Penetrating trauma has the highest risk
 May cause clinical pancreatitis
5. Following a surgery
 Abdominal or cardiothoracic

33. 6. Ampullary tumor
7. Drugs
•Rare
•Unknown predisposition
•Definitely as. :Valproic acid,azothioprine, thiazides
AND Probably as. : Asparaginase, cisplatin
8. Autoimmune
9. Hypercalcemia due to any cause
10.Toxins
11.Hereditary PRSS1
12.Vairal
13.Malnutrition
14.Idiopathic

34. Symptoms of acute pancreatitis
 Two extremes :WELL / IN Shock
 Pain : a cardinal symptom
 Site: epigastic, RUQ, diffuse
 Onset: sudden, reaches its max. within mins, then constant
 Character : dull
 Radiation: 50% to back. Others; chest
 Relieving factors: leaning forward(refractory to analgesics)
 Nausea
 Vomitting
 Retching
 Hiccoughs
 fever

35. Abdominal Examination
 Abdominal tenderness (diffuse,epigastric, RUQ)
 Palpable mass in epigastric area
 Decreased or absent bowel sounds (adynamic ileus)
 Guarding
 Biliary colic
 Jaundice if there’s obstruction of the bile duct
 Cullen’s sign
 GreyTurner’s Sign
 Fox’s sign

36. Sever disease:
 peritoneal signs
 ascites
 palpable abdominal mass
 GreyTurner’s sign
 Cullen’s sign
 and signs of hypovolemic shock

38. Fox’s
sign:
infra-
inguina
l
brusing
.

39. Investigations
LABs:
 CBC
 LFT
 Amylase and lipase
 ABGs
 Calcium
 Chemistry
 Serum lipids
AXR
U/S
CT scan

40. Aproach
 Patient’s history
 Physical examination
 Diagnostic findings
 Serum amylase levels greater than three times the
upper limit
 Serum amylase levels may be normal in patients with
pancreatitis related to alcohol abuse or
hypertriglyceridemia
 Levels greater than five times the top normal value
should be expected in patients with renal failure
because amylase is cleared by the kidneys

41.  Serum lipase is more sensitive and specific to the
pancreas
 An elevation of greater than three times the top
normal value usually confirms acute pancreatitis
 A lipase-to-amylase ratio of greater than 2 is usually
evident with pancreatitis related to alcohol abuse
 A rise in urine amylase and lipase can be expected and
are indicative of pancreatic damage
 Leukocytosis
 Hemoconcentration due to third space fluid loss
 Pancreatitis due to gallstones: elevated AST, ALT, and
lactate dehydrogenase

42. Imaging Modalities
 Plain abdominal x-rays:
Sentinel loop (most common finding on AXR)
Gallstones (10% only visible)
colon cut-off sign
 Abdominal ultrasound
 Cholelithiasis, biliary sludge, bile duct dilation, and
pseudocysts
 CT of abdomen
 MRCP (magnetic resonance
cholangiopancreatography)

43. Sentinel loop
Dilated segment of the
bowel

44. Gallstone

45. Colon cut-off sign
 abrupt termination
of gas within the
proximal colon at
the level of the
radiographic splenic
flexure, usually with
decompression of
the distal colon or
gas-filled
transverse colon
ending at the area
of pancreatic
inflammation

46. CT
 ascites, diffuse pancreatitis and gallbladder
distension with stones

47.  swelling of the head and body of the
pancreas with peripancreatic inflammatory
changes consistent with acute pancreatitis

48.  stranding around the head of the pancreas
suggestive of acute pancreatitis.

49. TRYTO ESTABLISHTHE ETIOLOGY
FIRST. DO NOT LABLE IT
IDIOPATHIC

50. Ranson’s Criteria
 The severity of acute pancreatitis is determined
by the existence of certain criteria, called
Ranson’s criteria
 The more criteria met by the patient, the more
severe the episode of pancreatitis
 1% mortality: fewer than three
 16%: three or four criteria
 40% with five or six criteria
 100%: seven or eight criteria

51. Ranson’s Criteria
 On admission
 Patient older than 55
 WBC > 16,000
 Serum glucose >200
 Serum lactate dehydrogenase >350
 Aspartate aminotransferase > 250
 During initial 48 hours after admission
 10% decrease in Hct
 BUN increase > 5
 Serum calcium < 8
 Base deficit > 4
 PaO2 < 60
 Estimated fluid sequestration > 6 liters

52. Common Complications of Acute
Pancreatitis
 Pulmonary
 Atelactasis
 Pleural effusions
 ARDS
 Cardiovascular
 Cardiogenic shock
 Neurologic
 Pancreatic
encephalopathy
Metabolic
Metabolic
acidosis
Hypocalcemia
Altered glucose
metabolism
Hematologic
DIC
GI bleeding
Renal
Prerenal failure

53. Chronic Pancreatitis

54.  Chronic inflammation of the pancreas causing
destruction of the parynchema, fibrosis and
calcification resulting in loss of both endo- and
exo- crine functions.
 Etiology :
 same as acute pancreatitis “pancreatitis associated
with gallstones predaminantly acute or relapsing-
acute”
 More idiopathic forms
 Calcific and Obstructive
 Alcoholic and non-Alcoholic

55.  Most common cause :
 In adults: alcohol intake
 In children: cystic fibrosis
 Idiopathic chronic pancreatitis is the leading cause
of nonalcoholic chronic pancreatitis
The events that initiate an inflamatory process are
still not well understood
In the alcohol-induced : suggested that the
primary defect may be the precipitation of
protein(inspissated enzyme )
In fact ,shown that alcohol has direct toxic effect
on the pancreas
Pathophysiology

56. Clinical features
 Clasic triad of pancreatic calcification , steatorrhea
, and diabetes mellitus .
 abdominal pain:
Two presentation:
 Episodes of acute inflammation in a previously injured
pancreas ( recurrent flare-ups)
 Chronic damage with persistent pain or malabsorption
(unrelenting pain)
 may be continuous, intermittent or absent
 Pattern is often atypical
 RUQ or LUQ of the back
 Diffuse throughout upper abdomen
 May be referred to the anterior chest or flank

57.  Typical form:
 Persistent , deep-seated,
 Unresponsive to antacids
 Worsened by alcohol intake or a heavy meal (especially fatty
foods)
 Often need narcotics
 Pancreatic insufficiency
 Weight loss
 Fat malabsorption:
 Steatorrhea: 15% of patients present with
steatorrhea and no pain
 Pancreatic diabetes:
 Like DM1 needs insulin , but risk of hypoglycemia is
more than it (because alfa cells is also affected
 Fat-soluble vitamin deficiency rare

58. Lab data
 Amylase and lipase : usually normal.Why?
 Classic triad “ pancreatic calcification , steatorrhea , and
diabetes mellitus “usually establishes chronic
pancreatitis
 Classic triad : found in fewer than one-third
 CBC ,electrolytes, and liver function tests are typically
normal
 Bilrubin and ALP may be increased
 Impaired glucose intolerance and elevated fasting blood
glucose
due to burned-
out pancreatitis

59.  Classic triad “ pancreatic calcification , steatorrhea ,
and diabetes mellitus “usually establishes chronic
pancreatitis
 Classic triad : found in fewer than one-third
 It is often necessary to perform secretin stimulation
test (abnormal when 60% or more of pancreatic
exocrine function has been lost)
 A decreased serum trypsinogen (<20ng/ml) or a fecal
elastase level of <100ug/mg of stool strongly suggests
severe pancreatic insufficiency

60. Imaging studies
KUB:
 Pancreatic
calcifications :
% 30
 most common
with alcoholic
pancreatitis,
but is also
seen in the
hereditary and
tropical forms
of the
disorder; it is
rare in
idiopathic
pancreatitis.

62. CT and MRI US
 calcifications
 ductal dilatation
 enlargement of the pancreas
 fluid collections (eg, pseudocysts)

65. ERCP
 Choice when calcifications are not present
and there is no evidence of steatorrhea.
 a normal study should not rule out the
diagnosis of chronic pancreatitis

66. ERCP
May provide useful information on the status of the
pancreatic ductal system
Abnormalities include :
1)luminal narowing
2)irregularitis in the ductal system with stenosis,
dilation,saculation,and ectasia
3)blockage of the duct by calcium deposits

67. Complications
 pseudocyst formation
 bile duct or duodenal obstruction
 pancreatic ascites or pleural effusion
 splenic vein thrombosis
 Pseudoaneurysms
 pancreatic cancer
 acute attacks of pancreatitis( particularly
alcoholics who continue drinking)

68. DIFFERENTIAL DIAGNOSIS
 Pancreatic cancer (most important)
 older age
 absence of a history of alcohol use
 weight loss
 a protracted flare of symptoms
 onset of significant constitutional symptoms
 pancreatic duct stricture greater than 10 mm in length on ERCP
 Markers such as CA 19-9 and CEA
 peptic ulcer disease
 gallstones
 irritable bowel syndrome
 Acute pancreatitis