This document provides an overview of chronic pancreatitis, including its definition, epidemiology, pathology, etiology, clinical features, complications, diagnosis, and treatment. Key points include: chronic pancreatitis results from permanent pancreatic damage and inflammation; common causes include alcohol abuse and genetic factors; complications involve pain, diabetes, maldigestion; diagnosis utilizes tests of pancreatic structure and function; treatment focuses on pain management, enzyme supplementation, and addressing underlying causes such as alcohol cessation.
3. DEFINITION :
Permanent & irreversible damage to pancreas with inflammation ,
fibrosis & gland destruction
Acute & Chronic pancreatitis
two ends of same spectrum
Histological evidence
without c/fs
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6. EPIDEMIOLOGY –
Alcohol abuse – 2/3rd of cases
Geographic variation
Mortality Rate – 3.6
Continued alcohol use – increased mortality risk by 60%
Cause of death – conditions
associated with smoking , alcoholism , pancreatic cancer
7. PATHOLOGY –
Interlobular fibrosis
Infiltration of lymphocytes , plasma cells & macrophages
Ducts – Eosinophilic plugs , dialation & strictures
Islets – involved very late in the course of disease
Calcified protein plugs – cause duct obstruction
8. Obstructive Chronic Pancreatitis –gland upstream of obstruction
Autoimmune Chronic Pancreatitis -
Positive for IgG4 staining
Obstructive phlebitis of major
and minor veins
Whirling fibrosis
Diffuse or segmental irregularity
& narrowing of pancreatic duct
9. PATHOPHYSIOLOGY –
Cellular necrosis & apoptosis
Fibrogenesis by stellate cells
PP OF ALCOHOLIC C.P. –
10% Of. heavy alcohol users
Alcohol Acetaldehyde in liver
Fatty Acid Ethanol Esters ( FAEE) in Pancreas
increase in IC Ca+ & Cell injury
19. 9. IDIOPATHIC CHRONIC PANCREATITIS –
Two types – Early onset & Late onset
EARLY ONSET ICP LATE ONSET ICP
Mean Age – 20 years 56 years
Gender Distribution – Equal Equal
Predominant c/f – Pain Exocrine & endocrine insufficiency
21. ABDOMINAL PAIN –
Epigastric,
deep boring & penetrating
worsened after a meal ,
relieved by sitting or leaning forward ,assuming knee chest position on one side & clasping knees onto
chest
Causes of pain –
1. tissue ischemia
2. Altered peripheral & central nociception
3. Complications
4. Hyperstimulation by CCK
22. STEATORRHEA –
lipase secretion is reduced to <10% of maximal output
Bulky foul smelling stools or passage of frank oil droplets
Vs small bowel diarrhea – No Watery diarrhea & abdominal cramps
Fat maldigestion earlier & severe compared to protein & carbohydrate maldigestion
R – 1. Lipase secretion decreases earlier
2. Lipase more sensitive to acid destruction & pancreatic proteases
3. Bile salt precipitation
Median time for development of exocrine insufficiency – 13 – 26 years
Weight loss – less common
23. Weight loss can occur with
1. painful flares
2. Small bowel bacterial overgrowth
3. Pancreatic or extrapancreatic malignancy
Fat soluble vitamin deficiencies – esp. Vit D def
24. DIABETES MELLITUS –
MC after pancreatic resection & tropical pancreatitis
Vs Type 1 or Type 2 DM –
1. Loss of hepatocyte insulin receptor Decreased hepatic
glucose output d/t IAPP
2. Decrease in stimulated glucagon secretion due to coexistent alpha cell injury
prolonged & severe hypoglycemia with insulin Rx
Mean time to development of DM - 19 – 26 years
27. PHYSICAL EXAMINATION IN CHRONIC PANCREATITIS –
Abdominal tenderness
Weight loss
Jaundice
Palpable spleen
Coexistent autoimmune features
28. DIAGNOSIS OF CHRONIC PANCREATITIS –
Two categories
1. Tests for pancreatic function
2. Tests for pancreatic structure
All diagnostic tests more accurate in far advanced disease
29. Functional abnormalities – Reduced maximal secretory capacity
Exocrine insufficiency
Endocrine insufficiency
Structural abnormalities - Main pancreatic duct
Side branches
Parenchyma
Classified as
Small duct disease Big duct disease
Normal / Equivocal on Imaging Abnormalities in duct on imaging
Functional abnormalities less common More common
MC Idiopathic MC d/t Alcohol abuse
Rx – Medical therapy Duct Decompression
30. TESTS FOR PANCREATIC FUNCTION –
Two types – Direct
Indirect
DIRECT TESTS –
Direct Hormonal stimulation – most sensitive
Mean peak bicarbonate conc. - > 80 mEq/L - N
Hormonal stimulation is more sensitive & specific than ERCP
Limitations - Not well standardized
Limited availability
Oroduodenal tube for an hour or more
31. INDIRECT TESTS –
Include Sr. Trypsinogen
Pancreatic enzymes in stool
Fecal fat excretion
Serum trypsinogen < 20 ng/mL in advanced chronic pancreatitis
False positive in Other malabsorptions , diarrheal diseases , severe malnutrition
Fecal Elastase < 200 microgm/ gm of stool
Fecal fat is measured over a 7 hr stool collection
N < 7% of ingested fat in stool
> 6 fat globules per hpf is abnormal
32. TESTS FOR PANCREATIC STRUCTURE –
1. Plain abdominal radiography –
Diffuse pancreatic calcification is specific
MC in alcoholic , late onset idiopathic , hereditary , tropical pancreatitis
2. Abdominal USG –
Difficult to distinguish age related variability form chronic pancreatitis
3. CT –
Grading can be done on CT / USG into Normal, Equivocal , Mild-moderate & Severe
33. Findings in chronic pancreatitis – Duct dilatation
Duct obstruction
Parenchymal heterogenity
Irregular contour
Calcification
4. MRI –
Duct Visualisation improved by secertin administration
5. ERCP –
Diagnostic as well as therapeutic
Risk - 5%
Diagnosis based on abnormalities in main pancreatic duct & side branches
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35. CHAIN OF LAKES Appearance
Changes similar can also be seen with normal ageing
CAMBRIDGE GRADING OF CHRONIC PANCREATITIS ON ERCP
GRADE MAIN PANCREATIC DUCT SIDE BRANCHES
NORMAL Normal Normal
EQUIVOCAL Normal <3 Abnormal
MILD Normal >/= 3 Abnormal
MODERATE Abnormal “
SEVERE Abnormal with
Large cavity >10mm)
Obstruction
Filling defects
Severe dilatation /
irregularity
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36. 6. ENDOSCOPIC USG –
Presence of >/= 3 features is positive
Rosemont criteria -
Score >5 highly specific
Score of 3 or 4 is indeterminate
EUS abnormalities in chronic pancreatitis -
PARENCHYMAL ABNORMALITIES DUCTAL ABNORMALITIES
Hyperechoic foci Main duct dilatation & irregularity
Hyperechoic strands Hyperechoic ductal walls
Lobularity of contour Visible side branches
Cysts Calcification
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38. DIAGNOSTIC STRATEGY IN CHRONIC PANCREATITIS –
In patients with pain as primary complaint & suspected chronic pancreatitis
High quality multidetector CT / MRI With MRCP is best initial diagnostic test
If nondiagnostic , Hormal stimulation direct pancreatic testing , If unavailable , EUS
If exocrine or endocrine insufficiency is suspected
Fecal Elastase / Serum Trypsinogen / USG / CT
39. TREATMENT -
1. ABDOMINAL PAIN
associated conditions
- Pancreatic pseudo cyst
- Duodenal & bile duct compression
- Superimposed pancreatic cancer
- Gastroparesis
Identify patients with big duct pancreatitis
MEDICAL THERAPY –
1. Analgesics
2. Cessation of Alcohol & Tobacco
3. Antioxidants
4. Pancreatic enzyme therapy
5. Octreotide
40. ANALGESIA –
acetaminophen or aspirin
narcotic analgesics
Propoxyphene or Tramadol
Coexistence depression lowers pain threshold
TCAs
SSRIs
SNRIs
Voltage gated N type Ca channel inhibitors.
42. PANCREATIC ENZYME THERAPY –
- deliver proteases to duodenum or very proximal jejunum
- Enteric coated preparations may not release majority of proteases until they reach the
more distal small bowel
- Non Enteric coated preparations
- Non enteric coated enzymes cinactivated by gastric acid , concomitant use of
acid suppressant
- Enzyme therapy is not successful in pain a/w big duct chronic pancreatitis
43. OCTREOTIDE –
- Reduces pancreatic secretion & circulating CCK levels
- It also has some direct anti nociceptive effect
ENDOSCOPIC THERAPY –
- Most appropriate in patient with dominant stricture & ductal stone
- Options include
Pancreatic duct Sphincterotomy
Stent Placement
Pancreatic duct stone removal
I
44. SURGICAL THERAPY –
- Considered for intractable pain abdomen with failed medical therapy
- Other indications
Other organ involvement
Failure of endoscopic therapy for pseudo cysts
Internal pancreatic fistulas
Exclusion of malignancy
- For pain , Pancreatic duct drainage
Resection of all or part of pancreas
NERVE BLOCK & NEUROLYSIS –
- Celiac plexus block with a glucocorticoid & LA Under
- Celiac plexus neurolysis with absolute alcohol EUS or CT guidance
45. 2. TREATMENT OF MALDIGESTION & STEATORRHEA –
- 30,000 IU / 90,000 USP of lipase with prandial & postprandial
portion of each meal
- Concomitant acid suppression with H2RA or PPI necessary with enteric coated tablets
- Clinical parameters to gauge the effectiveness of enzyme supplementation
Improvement in stool consistency
Loss of visible fat in stool
Gain in body weight
- periodically evaluate for fat soluble vitamin deficiencies especially Vitamin D
- BMD assessment for osteopenia is necessary
- Causes for failure of enzyme therapy
Inadequate dose d/t Patient Noncompliance ( MC cause ) Have patient
eat more frequent , small meals
46. - If. fail , search for an alternative cause for malabsorption
- If all measures fail , replace diet fat with medium chain TGs
47. 3. TREATMENT OF DIABETES MELLITUS –
- Therapy is directed at control of urinary losses of glucose
- Insulin requirement is lower than that with T1 DM patients
- Overvigorous BG control are a/w hypoglycemia
- Tight BG control are indicated in patients with hyperlipidemic
pancreatitis
48. TREATMENT OF AUTOIMMUNE PANCREATITIS –
- Glucocorticoids have clinical , histolopathological & morphological efficacy
- Start with Prednisone at 40 mg/ day for 4 weeks
- Parameters to be followed include
Symptomatic relief
Serial changes in pancreas & bile ducts on imaging
Reduced serum gamma globulin & IgG4 levels
Improvement in liver tests
- Poor response to GCs in 2 to 4 weeks should raise the suspicion of pancreatic cancer or
other causes of Chronic pancreatitis
- For relapse , agents useful are
6- Mercaptapurine , Azathioprine , Rituximab, Cyclosporine & Cyclophosphamide
49. REFERENCES –
- Sleisenger & Fordtran GI and Liver Disease , 9th Ed
- Harrison Principles of Internal Medicine 19th Ed