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home - Pancreas - Pancreatitis - Chronic Pancreatitis Diagnosis Written by Dr Sebastian Zeki

Knows the aetiology of acute pancreatitis Understands the means by
which the condition is diagnosed

Is aware of the risk stratification and prognostic scoring systems such
as Glasgow and Ranson; can apply this to the
management plan for individual patients

Knows the complications of severe attacks and the indications for

Knows how to initiate investigation of patients with recurrent
unexplained attacks of pancreatitis

Shows ability to make early risk stratification and involve multidisciplinary team and/or intensive care staff when appropriate

Collaborates closely with radiological and surgical colleagues where

Transfers patient to a specialist centre in accordance with guidelines



Understands the causes presentation investigation and
management of chronic pancreatitis

Knows the potential value of the various imaging modalities
Recognises the potential of blood and stool tests

Aware of the exocrine and endocrine consequences of the condition
Recognises complications

Knows the value of endoscopic non-invasive (ESWL) and surgical

Can diagnose the condition promptly
Knows possible avenues of treatment both to treat the consequences
of pancreatic insufficiency and to control pain where appropriate

Can recognise complications
Works within multi-disciplinary team and liaises with colleagues in
pain management

Shows empathy with patient and relatives


Chronic Pancreatitis Diagnosis

Toxic- Metabolic Hyper (triglyceride/ PTH) Medications* ToxinsIdiopathic (tropical 20%. Tropical most common cause in S. India/ usually affect kids who die in early adulthood. SPINK1 mutations and cassava fruit independently implicated)GeneticHereditary pancreatitisPRSS1- AD. Presents in childhoodSPINK1- 40% get pancreatic Ca by age 70CF AutoimmuneRecurrent and severe acute pancreatitis Postirradiation Postnecrotic (severe acute pancreatitis) Recurrent acute pancreatitis Vascular ischemiaObstruction of duct (eg trauma/ structural problems/ tumours/ stones/ SOD) ETOH 10% get CP75% of CP due to alcohol. Linear relationship to amount of EtOH drunk. Get increased basal secretion of pancreatic secretion and more sensitive to CCK Protein 1. Increased protein secretion (mainly GP2)2. Protein plug acts as nidus for calcification3. Stone causes inflamm-tion and cell loss Ca++ Ca++ Ca++ Ca++ Ca++ Ca++ 1. 2. 3. 1.Proteinaceous ductal plugs 2.Ischemia — 3. Antioxidants — Theories of Pathogenesis of Chronic Pancreatitis 1. PRSS1 (serine protease 1 gene) — Most common genetic cause- present in up to 75%. 2. SPINK1 — (serine protease inhibitor Kazal type 1) 3. CFTR 3 patterns:a) Homozygotes for severe CFTR mutations (typical CF) — Get classic cystic fibrosis without pancreatic insufficiency. b) Compound heterozygotes in which one or both CFTR mutations are mild (atypical CF) — Lack chronic sinopulmonary diseaseMay have normal sweat chloride testingMay also have congenital absence of the vas deferens. The risk for chronic pancreatitis is increased 60x.c) Heterozygotes (CFTR mutation carriers) — Increased risk 3-4x. 4. Hereditary Pancreatitis =Any autosomal dominant pancreatitisHigh penetrance-80% with the inherited defect develop chronic pancreatitis by age 20 years.Usually PRSS1Age: 10-12Presentation: Severe acute pancreatitis. Develop chronic calcif pancreatitisA strong association with pancreatic cancer. PRSS1 (serine protease 1 gene) Encodes cationic trypsinogen Mutations enhance activation or decrease inactiva-tion allowing pancreatic autodigestion R122H and N29I mutations are the most common SPINK1 — (serine protease inhibitor Kazal type 1) AR A pancreatic trypsin inhibitor Mutations in SPINK1 increase the risk for chronic pancreatitis about 12-fold over the general population.Only 1% of carrier get CP so is probably disease modifier AD Chronic Pancreatitis Causes (TIGAROE) Written by Dr Sebastian Zeki

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