Definition/General
Introduction:
Pancreatitis represents inflammatory disease of the pancreas with characteristic FNAC findings
Can be acute or chronic in nature
FNAC shows inflammatory cells and reactive changes
Important to distinguish from neoplastic lesions
May present as mass-forming pancreatitis.
Origin:
Results from pancreatic enzyme activation within the gland
Leads to autodigestion and inflammation
Acute pancreatitis: reversible inflammatory process
Chronic pancreatitis: progressive fibrosis and dysfunction
Various etiologies trigger the inflammatory cascade.
Classification:
Acute pancreatitis: interstitial edematous
Acute pancreatitis: necrotizing
Chronic pancreatitis: obstructive type
Chronic pancreatitis: inflammatory type
Autoimmune pancreatitis (IgG4-related)
Hereditary pancreatitis.
Epidemiology:
Common cause of pancreatic masses
Peak incidence 4th-5th decades
Male predominance in chronic pancreatitis
Alcohol-related most common cause
Gallstone pancreatitis in females
Indian population: tropical pancreatitis seen.
Clinical Features
Presentation:
Abdominal pain (most common symptom)
Epigastric pain radiating to back
Nausea and vomiting
Weight loss (chronic cases)
Steatorrhea (exocrine insufficiency)
Diabetes mellitus (endocrine insufficiency).
Symptoms:
Severe epigastric pain (acute cases)
Chronic dull aching pain
Post-prandial exacerbation
Nausea and vomiting
Weight loss and malnutrition
Steatorrhea and flatulence
New-onset diabetes.
Risk Factors:
Alcohol abuse (most common cause)
Gallstones
Hypertriglyceridemia
Hereditary factors (PRSS1, CFTR mutations)
Medications
Trauma
Tropical pancreatitis (malnutrition-related).
Screening:
Serum amylase and lipase (elevated acutely)
CT scan for morphological assessment
MRCP for ductal evaluation
EUS for detailed pancreatic imaging
Fecal elastase for exocrine function.
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Gross Description
Appearance:
Acute: enlarged, edematous pancreas
Hemorrhagic areas in necrotizing pancreatitis
Chronic: firm, nodular surface
Calcifications visible in chronic cases
Ductal dilatation and strictures.
Characteristics:
Acute: soft, edematous consistency
Areas of fat necrosis
Hemorrhage and necrosis
Chronic: hard, fibrotic texture
Gritty calcifications
Dilated main pancreatic duct.
Size Location:
Diffuse involvement common
Head more affected in chronic disease
Mass-forming pancreatitis may simulate tumor
Can involve entire gland or be segmental.
Multifocality:
Usually diffuse process
Focal areas more severely affected
Pseudocyst formation in severe cases
Skip lesions in chronic pancreatitis
Strictures and dilatations alternate.
Microscopic Description
Histological Features:
Acute: interstitial edema and inflammatory infiltrate
Neutrophilic infiltration predominant
Fat necrosis and hemorrhage
Chronic: chronic inflammatory cells
Fibrosis and acinar atrophy
Ductal proliferation.
Cellular Characteristics:
Acute: neutrophils and macrophages
Reactive ductal epithelium
Chronic: lymphocytes and plasma cells
Activated fibroblasts
Reactive/regenerative epithelial changes
Loss of acinar cells.
Architectural Patterns:
Loss of normal acinar architecture
Fibrotic replacement (chronic)
Ductal dilatation and metaplasia
Pseudocyst formation
Vascular changes and thrombosis.
Grading Criteria:
Acute: mild, moderate, severe based on necrosis extent
Chronic: early, advanced stages
Cambridge classification for chronic pancreatitis
Functional assessment important.
Immunohistochemistry
Positive Markers:
CK19 (ductal epithelium)
CK7 (reactive ducts)
Trypsin (residual acinar cells)
Chromogranin A (islet cells)
Smooth muscle actin (myofibroblasts)
IgG4 (autoimmune pancreatitis).
Negative Markers:
CEA (helps exclude adenocarcinoma)
CA 19-9 (may be elevated but non-specific)
p53 (typically negative, unlike carcinoma)
SMAD4 (retained, unlike ductal adenocarcinoma).
Diagnostic Utility:
IgG4 staining diagnostic for autoimmune pancreatitis
p53 and SMAD4 help exclude carcinoma
Ductal markers show reactive changes
Combined clinical-pathological correlation essential.
Molecular Subtypes:
Type 1 autoimmune pancreatitis (IgG4-related)
Type 2 autoimmune pancreatitis (idiopathic)
Hereditary pancreatitis (genetic mutations)
Tropical pancreatitis (nutritional).
Molecular/Genetic
Genetic Mutations:
PRSS1 mutations (hereditary pancreatitis)
CFTR mutations (cystic fibrosis-related)
SPINK1 mutations
CTRC mutations
CPA1 mutations
CEL gene mutations.
Molecular Markers:
Inflammatory cytokines elevated
Oxidative stress markers
Fibrosis-related genes upregulated
Growth factors (PDGF, TGF-beta)
Matrix metalloproteinases.
Prognostic Significance:
Genetic testing important for hereditary cases
Risk of pancreatic cancer in chronic pancreatitis
Functional outcomes depend on extent of damage
Early intervention improves prognosis.
Therapeutic Targets:
Anti-inflammatory agents
Antioxidants
Enzyme replacement therapy
Pain management
Pancreaticoenteric drainage
Total pancreatectomy with islet transplant (severe cases).
Differential Diagnosis
Similar Entities:
Pancreatic ductal adenocarcinoma (most important)
Autoimmune pancreatitis
Neuroendocrine tumor
Chronic pancreatitis vs carcinoma
Groove pancreatitis.
Distinguishing Features:
Pancreatitis: inflammatory cells predominant
Pancreatitis: Reactive epithelial changes
Carcinoma: malignant epithelial cells
Carcinoma: p53 positive, SMAD4 loss
Clinical correlation essential.
Diagnostic Challenges:
Mass-forming pancreatitis vs carcinoma most difficult
Sampling adequacy crucial
May require multiple FNACs
Core biopsy sometimes needed
Clinical and imaging correlation mandatory.
Rare Variants:
Autoimmune pancreatitis (IgG4-related)
Groove pancreatitis
Paraduodenal pancreatitis
Tropical pancreatitis
Hereditary pancreatitis.
Sample Pathology Report
Template Format
Sample Pathology Report
Complete Report: This is an example of how the final pathology report should be structured for this condition.
Specimen Information
FNAC from pancreatic lesion, [location], [number] passes
Adequacy
Specimen is adequate for evaluation
Cellular Findings
Smears show [inflammatory cell types] with [epithelial changes]
Inflammatory Pattern
Predominantly [acute/chronic] inflammatory pattern
Epithelial Changes
Reactive ductal epithelium showing [describe changes]
Background
Background shows [debris/necrosis/blood]
Malignant Cells
No malignant cells identified
Final Diagnosis
FNAC pancreas: Findings consistent with pancreatitis