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Kurdistan Board GEH J Club
Supervisor:
Dr.Mohamed Alshekhani.
Definition:
• A wide range of progressive fibro-inflammatory diseases of
the exocrine pancreas that eventually lead to damage of
the gland,causeing failure of exocrine&endocrine
pancreatic function needing treatment.
• Classified into three forms:
• Chronic calcifying pancreatitis(most common).
• Chronic obstructive pancreatitis.
• Steroid-responsive pancreatitis (chronic AIP).
• The natural history&clinical presentation vary depending
on the form & causal mechanism, although abdominal pain
is present in most patients.
Definition:
• Early stages characterised by clinically apparent acute
pancreatitis.
• As the disease progresses, there is development of
intraductal stones (in MPD or side branches), pancreatic
ductal distortion, strictures&pancreatic calcification.
• Extensive destruction of the pancreatic parenchyma leads
to steatorrhoea &diabetes.
• Obstructive, autoimmune; very rarely include calcification.
Definition:
• Chronic obstructive pancreatitis results from primary
injury to the duct or partial or complete ductal obstruction.
• Obstructive pancreatitis occurs upstream from a
pancreatic duct stricture caused by pancreatic duct injury
(during endoscopic or surgical procedures, after
necrotising acute pancreatitis, or blunt abd injury);
narrowed pancreatico-enteric anastomoses; & tumours
obstructing (eg, ductal adenocan & IPMN).
• Ductal obstruction due to strictures&stones can also
complicate chronic calcifying pancreatitis.
• In the pure form, only the organ upstream from the obst is
affected, with the downstream pancreas being healthy.
• Chronic obstructive pancreatitis is often asymptomatic;
however, partial obstruction can lead to recurrent bouts of
clinically AP involving the obstructed part of the gland.
Definition:
• Steroid-responsive pancreatitis (chronic AIP), better AIP,
the inflammation responds rapidly to corticosteroids.
• AIP classified into two subtypes:
• Type 1 & type 2, two distinct diseases.
• Type 2 AIP better called idiopathic duct-centric chronic
pancreatitis.
Git j club chronic pancreatitis 16.
Definition:
• T1AIP is the pancreatic manifestation of a multiorgan fibro-
inflammatory syndrome known as immunoglobulin G4
(IgG4)-related disease, characterised by increased serum
IgG4, multiorgan involvement, typical histological signs&
rapid response to CSs& B-cell depletion therapy.
• IgG4-related disease affects several organs;pancreas, bile
duct, salivary glands, retroperitoneum, kidneys& LNs.
• Pancreatic disease in T1AIP resembles that seen in other
organs affected characterised by a dense lympho
plasmacytic infiltrate around medium-sized ducts, a
peculiar swirling (storiform) fibrosis, an intense infl
ammation that surrounds veins (obliterative phlebitis) &
spares adjacent arteries&abundant (>10 per high-power
field) IgG4-positive plasma cells.
Definition:
• The most common clinical presentation is obstructive
jaundice mimicking pancreatic cancer; it less commonly
presents with clinically acute pancreatitis.
• Pain is not a prominent feature &if present, resolves
quickly with steroid
• Pancreatic calcification is uncommon &usually occurs in
relapsing disease.
Definition:
• Idiopathic duct-centric chronic pancreatitis (T2QIP) differs
substantially T1AIP. Histologically, characterised by
neutrophilic infiltrate in the pancreatic duct epithelium (a
granulocyte epithelial lesion), which can lead to ductal
obliteration.
• Tends to present with pancreatitis, often recurrent.
• Pancreatic fibro-atrophy can be associated with intense
bland fibrosis, typically noninfl ammatory, not associated
with the pancreatic ductal changes commonly seen in
chronic pancreatitis.
Git j club chronic pancreatitis 16.
Epidemiology:
• Incidence in Europe ;4-13/100 000
• Prevalence 41.76 / 100 000).
• Men have a higher incidence & Black higher risk.
Risk factors:Alcohol
• The causative agent in nearly 50%
• Major risk factor in 43%, either alone (34%) or in
combination with ductal obstruction (9%).
• More frequently in men (59%) than in women (28%).
• Genetic variants in the CLDN2 gene loci have influence the
risk ,higher in men than in women.
• Alcohol increases the risk in a dose-dependent manner,
doubles or trebles at a threshold of four or five drinks/ day.
• The incidence in regular excess consumers is low (5–15%)
• It is unclear whether there is truly any safe threshold of
alcohol intake in relation to chronic pancreatitis.
• Pathogenesis:chronic alcohol sensitises the acinar cell to
injury by interfering with mechanisms protecting against
stress induced by the endoplasmic reticulum.
Risk factors:smoking
• An independent risk facto.
• The pooled risk estimate 2.5, dose-dependent&synergistic
with alcohol.
• Smoking as the strongest risk factor for progression from
acute to chronic pancreatitis.
• Nicotine induces oxidative stress in the pancreatic acini.
• The nicotine metabolite 4-(methylnitrosamino)-1-(3-
pyridyl)-1-butanone (NNK) has been implicated.
Risk factors:genetics
• Either by premature activation of trypsinogen or failure to
inactivate trypsin during pancreatic inflammation.
• Gain-of-function mutations in the cationic trypsin gene
(PRSS1) lead to premature trypsinogen activation as the
cause of hereditary pancreatitis.
• Inheritance is autosomal-dominant with high penetrance,
• Mutation in SPINK1 is not an independent risk factor but, it
has disease-modifying properties implicated in the
progression of recurrent acute pancreatitis to chronic
pancreatitis& associated with tropical calcific pancreatitis.
• Mutations in CFTR identified without pulmonary
manifestations of CF& coinheritance with SPINK1 incr
risk .
• CTRC, CASR, CLDN2 on X ch, associated with CP.
• Hereditary pancreatitis secondary to PRSS1 mutation is
Risk factors:ductal obstruction
• Ductal obstruction due to inflammatory strictures, benign
tumours, or malignancies leads to chronic obstructive
pancreatitis upstream from the obstruction.
• Occasionally chronic pancreatitis might beconfined to the
dorsal pancreas in patients with pancreas divisum,
suggesting a causative role of ductal obstruction
• A higher frequency of pancreas divisum has been noted in
patients with CFTR mutation-associated pancreatitis
Risk factors:idiopathic
• Large proportion.
• Before labelling idiopathic, thorough investigation is
warranted.
• Tropical pancreatitis, or fibrocalculous pancreatic, is a
form the tropics, specially Southern India characterised by
early-onset pain, large MPD calcification& rapid onset of
ketosis-resistant diabetes.
• Although genetic SPINK1, nutritional&inflaammatory
factors have been implicated.
Risk factors:pathogenesis
• Protein-rich plugs form in the interlobular & intralobular
ducts secondary to a failure in the compensatory increase
of ductal bicarbonate secretion, which results in a viscous
ductal microenvironment.
• Ductal obstruction results in inflammation, which
subsequently leads to pancreatic parenchymal fibrosis.
• Ducts bstruction lead to pancreatic ductal hypertension
with resultant hypoperfusion & ischaemic injury of acini.
• ? A sentinel event of AP is a key element.
• Pancreatic stellate cells can be activated (to form collagen
&extracellular matrix, causing pancreatic parenchymal
fibrosis) by chemokines as TGFβ ,PDGF released by
pancreatic inflammation.
Risk factors:Clinical features
• Patients do not usually present with classic signs.
• More often, patients present with recurrent clinically acute
pancreatitis.
• Over a varying time-interval (years - decades) progressive
changes appear in the pancreas.
• Initially such changes are visible only on endoscopic
ultrasound.
• Eventually, patients develop the clinical triad of abdominal
pain, exocrine pancreatic insufficiency&diabetes.
• Pain is often the over-riding symptom&present in up to
85%.
• Exocrine insuff manifests as steatorrhoea&in severe
cases, wt loss,malnutrition&fat-soluble vit deficiency.
Risk factors:Clinical features
• Endocrine insufficiency results in pancreatogenous
diabetes, T3C DM to distinguish it from T1&T2DM.
• Pain is usually post-prandial, epigastric with radiation to
back, often with nausea /vomiting,partially relieved by
sitting or leaning forward ,but the location, severity,
character, intensity are highly variable.
Risk factors:Clinical features
• The mechanism of pain is poorly understood:
• 1. Pancreatic ductal& parenchymal hypertension.
• 2. Activation of intrapancreatic nociceptors, hypertrophy &
inflammation of intrapancreatic nerves& abnormal pain
processing in CNS.
• 3.Intrapancreatic neural remodelling&similar changes in
the viscerosensory cortex are key factors evidenced by
poor correlation bet structural changes &severity of pain&
pain persistence in total pancreatectomy.
Risk factors:Clinical features
• The clinical hallmark of pancreatic exocrine insufficiency is
steatorrhoea that does not usually occur until pancreatic
lipase output drops below 10–15% normal.
• So maldigestion /steatorrhoea are of advanced stages.
• The appearance of the stool is an unreliable predictor of
steatorrhoea & 72 h faecal fat estimation, done when the
patient is taking a diet restricted to 100 g of fat per day, is
often required to establish diagnosis.
• In the absence of other clinical / radiological features,
isolated steatorrhoea is almost never secondary to CP.
Risk factors:Clinical features
• Most patients eventually develop T3CDM, but CP can occur
with T1&T2DM.
• A history of long-standing CP before the onset of diabetes
is usually typical for diagnosis of T3CDM.
• Patients are at a higher risk of hypoglycaemia due to
concomitant loss of counter-regulatory hormones
glucagon & pancreatic polypeptide.
• Common complications:pseudocysts; CBD stricture;
duodenal stenosis; pleural effusion; PVT; SPT with
formation of gastric varices; pseudoaneurysm affecting the
splenic, hepatic, gastroduodenal& pancreaticoduodenal
arteries& pancreatic ascites
• CP at a higher risk of pancreatic adenocan ,greatest for
early-onset in patients with hereditary&tropical CP.
Diagnosis
• Often obvious in advanced cases.
• In early stage diagnosis is challenging& often based on a
combination of clinical, imaging &pancreatic funct testing.
• In the absence of established diagnostic criteria, early
diagnosis remains an elusive diagnosis.
Diagnosis
• Histology:
• Fibrosis,parenchymal loss, lobular inflammation&ductal
changes are key diagnostic histological features.
• In late burntout CP, inflammation might be absent.
• In autopsy pancreatic fibrosis is common in asymptomatic
people &DM, so fibrosis alone is insufficient for diagnosis.
• Sampling error is a major limitation for surgical and
endoscopic biopsies &false-negative results.
• There is also a risk of causing pancreatitis by EUS-FNA.
• Overall, histology is rarely used to establish diagnosis.
Git j club chronic pancreatitis 16.
Diagnosis
• CT & MRCP are reasonably sensitive for detection of
advanced CP, but sensitivity is low.
• IV secretin during MRCP increases sensitivity to detect
ductal changes
• With EUS, ERP no longer used for diagnosis.
• The ductal changes noted on ERP (Cambridge
classificationis), was considered the most reliable imaging
test with sensitivity up to 90%.
Diagnosis
• The Rosemont EUS criteria for diagnosis combine ductal
&parenchymal features; 4 categories:
• Consistent,suggestive, indeterminate & healthy.
• The Japanese EUS criteria include a category of early CP.
• Sensitivities / specificities of > 80% to diagnose pancreatic
fibrosis reported for EUS.
• Concomitant presence of four or more EUS criteria has a
sensitivity of up to 91%.
• Pancreatic changes on EUS can also be seen in patients
with no symptoms of pancreatic disease; so findings
should always be interpreted in the appropriate clinical
context & are rarely diagnostic of chronic pancreatitis in
isolation.
Diagnosis
• Pancreatic function tests are classified as direct&indirect.
• Direct pancreatic function tests have been phased out of
clinical practice.
• At some centres the secretin function test has been
combined with EUS in which pancreatic fluid is collected
endoscopically after secretin stimulation, allowing for a
structural assessment of the pancreas at the same time,
but not yet widely used.
Diagnosis
• Indirect pancreatic function tests include measurement of
faecal elastase 1 & faecal fat.
• A faecal elastase 1 > 100 μg/g of stool is used as a marker
of pancreatic exocrine dysfunction.
• The test result can be erroneously low with diarrhoea.
• Faecal elastase 1 can be checked easily &not affected by
concomitant panc enzyme replacement, so commonly
used,but has low sensitivity& specificity in early disease &
can have high false-positive with up to 10%.
• 72 h faecal fat is cumbersome& not done at most centres.
• Despite its limitations it is fairly reliable if done properly.
• At present no single test in isolation is diagnostic.
• Abns on EUS&PFTs in the absence of signs/ symptoms are
not specific&should not be used for diagnosis.
Management: Medical
• Management of ;
• Pain.
• Exocrin einsufficiency.
• Endocrine insufficiency.
• Complications (biliary obstruction, bleeding, or
malignancy).
Management: Medical
• Nutrition& lifestyle modification are key components.
• Endoscopic/surgical interventions have a role in some.
• Pain control is the most difficult challenge.
• Long-term use of opioids is best avoided.
• Adjunctive pain medication as TADs,gabapentin,
pregabalin&SSRIs have been used either alone or in
combination with opioids with variable results.
• Tramadol have a similar efficacy with less side-effects.
• Pan enzymes, octreotide, montelukast,antioxisants &
allopurinol are not effective for pain.
• Alcohol & smoking cessation can reduce pain.
• Contributing factors looked for (pseudocysts, duod
strictures& trt-related complications as opioid-induced
bowel dysfunction or postop intra-abdominal adhesions).
Management: endoscopic
• The common clinical indications for endoscopic
intervention:
• 1.Intraductal stones in the region of the pancreatic head,
• MPD stricture
• Symptomatic pseudocyst.
• Large stones usually need (ESWL).
• ESWL + ERCP have not shown any added benefit.
• Dominant strictures in MPD are managed by endoscopic
pancreatic single stent long term.
• EUS-CPN relieves pain in about 50% of patients, the effect
lasts a maximum of a few weeks & not recommended for
patients with painful CP without concomitant pan can.
Management: endoscopic
• In patients with pancreas divisum& recurrent pancreatitis,
risks of minor papilla sphincterotomy (stenosis/ thermal
duct injury) should be weighed against the potential
prevention of recurrence, less helpful in established CP
than recurrent AP.
• Long-term pancreatic duct stenting induces morphological
changes in MPD&parenchymal changes resembling CP&
should be avoided in patients with pancreas divisum.
Management: surgical
• Surgical intervention is effective in carefully selected.
• Common indications:
• Poorly controlled pain
• Duodenal, biliary &pancreatic duct obstruction;
• Symptomatic pseudocysts
• Suspicion of cancer.
• Surgery classified into 3:
• Drainage procedures
• Partial pancreatic resection
• Total pancreatectomy
Management: pancreatic enzymes replacement
• Treatment is often started at lower dose with 40 000–50 000
USP units of lipase with each meal & half that amount with
snacks.
• Lower doses of 25 000–40 000 units per meal might be
effective& should be started at a low dose& titrated on the
basis of clinical response.
• Digestion calories should be equally divided 3-5 meals/day
&enzyme pills distributed through the meal.
• If there is no improvement in steatorrhoea at maximum
doses,PPI+ alternative causes of diarrhoea explored.
• The monitoring of serum fat-soluble vitamins A, D, and E
&appropriate supplementation is important.
Management: pancreatic endocrine insufficiency
• Lifestyle modification is a key component of treatment.
• Metformin is often the firs tline drug.
• In time most patients need insulin therapy,but more prone
to hypoglycaemia & need closely monitoring &insulin
pump is often the safest & most effective.
• The importance of smoking & alcohol abstinence, healthy
eating habits& daily exercise is often underemphasised.
• Referral to formal structured de-addiction programmes& a
nutritionist should be considered when appropriate.
Git j club chronic pancreatitis 16.
What are arrows?
Endoscopic Ultrasound
Diffuse hypoechoic enlargement of pancreas. Fine needle
aspirate of the pancreas was negative for tumor.
ERCP
There was a long segment of extrahepatic biliary stricture.
The pancreatic duct was normal in size but irregular.
Brushings, biopsies and bile aspirate were negative for
tumor
Git j club chronic pancreatitis 16.
Git j club chronic pancreatitis 16.
Git j club chronic pancreatitis 16.
Git j club chronic pancreatitis 16.
Git j club chronic pancreatitis 16.
Git j club chronic pancreatitis 16.
Abstract:
• Chronic pancreatitis describes a wide spectrum of
fibro-inflammatory disorders of the exocrine
pancreas that includes calcifying, obstructive&
steroid-responsive forms.
• Epidemiology: incidence seems to be on the rise.
Smoking, drinking alcohol& genetic predisposition
are the major risk factors.
• Management is focusing on pain management, the
role of endoscopic & surgical intervention& the
use of pancreatic enzyme-replacement therapy.
• Management of patients is often challenging &
necessitates a multidisciplinary approach.

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Git j club chronic pancreatitis 16.

  • 1. Kurdistan Board GEH J Club Supervisor: Dr.Mohamed Alshekhani.
  • 2. Definition: • A wide range of progressive fibro-inflammatory diseases of the exocrine pancreas that eventually lead to damage of the gland,causeing failure of exocrine&endocrine pancreatic function needing treatment. • Classified into three forms: • Chronic calcifying pancreatitis(most common). • Chronic obstructive pancreatitis. • Steroid-responsive pancreatitis (chronic AIP). • The natural history&clinical presentation vary depending on the form & causal mechanism, although abdominal pain is present in most patients.
  • 3. Definition: • Early stages characterised by clinically apparent acute pancreatitis. • As the disease progresses, there is development of intraductal stones (in MPD or side branches), pancreatic ductal distortion, strictures&pancreatic calcification. • Extensive destruction of the pancreatic parenchyma leads to steatorrhoea &diabetes. • Obstructive, autoimmune; very rarely include calcification.
  • 4. Definition: • Chronic obstructive pancreatitis results from primary injury to the duct or partial or complete ductal obstruction. • Obstructive pancreatitis occurs upstream from a pancreatic duct stricture caused by pancreatic duct injury (during endoscopic or surgical procedures, after necrotising acute pancreatitis, or blunt abd injury); narrowed pancreatico-enteric anastomoses; & tumours obstructing (eg, ductal adenocan & IPMN). • Ductal obstruction due to strictures&stones can also complicate chronic calcifying pancreatitis. • In the pure form, only the organ upstream from the obst is affected, with the downstream pancreas being healthy. • Chronic obstructive pancreatitis is often asymptomatic; however, partial obstruction can lead to recurrent bouts of clinically AP involving the obstructed part of the gland.
  • 5. Definition: • Steroid-responsive pancreatitis (chronic AIP), better AIP, the inflammation responds rapidly to corticosteroids. • AIP classified into two subtypes: • Type 1 & type 2, two distinct diseases. • Type 2 AIP better called idiopathic duct-centric chronic pancreatitis.
  • 7. Definition: • T1AIP is the pancreatic manifestation of a multiorgan fibro- inflammatory syndrome known as immunoglobulin G4 (IgG4)-related disease, characterised by increased serum IgG4, multiorgan involvement, typical histological signs& rapid response to CSs& B-cell depletion therapy. • IgG4-related disease affects several organs;pancreas, bile duct, salivary glands, retroperitoneum, kidneys& LNs. • Pancreatic disease in T1AIP resembles that seen in other organs affected characterised by a dense lympho plasmacytic infiltrate around medium-sized ducts, a peculiar swirling (storiform) fibrosis, an intense infl ammation that surrounds veins (obliterative phlebitis) & spares adjacent arteries&abundant (>10 per high-power field) IgG4-positive plasma cells.
  • 8. Definition: • The most common clinical presentation is obstructive jaundice mimicking pancreatic cancer; it less commonly presents with clinically acute pancreatitis. • Pain is not a prominent feature &if present, resolves quickly with steroid • Pancreatic calcification is uncommon &usually occurs in relapsing disease.
  • 9. Definition: • Idiopathic duct-centric chronic pancreatitis (T2QIP) differs substantially T1AIP. Histologically, characterised by neutrophilic infiltrate in the pancreatic duct epithelium (a granulocyte epithelial lesion), which can lead to ductal obliteration. • Tends to present with pancreatitis, often recurrent. • Pancreatic fibro-atrophy can be associated with intense bland fibrosis, typically noninfl ammatory, not associated with the pancreatic ductal changes commonly seen in chronic pancreatitis.
  • 11. Epidemiology: • Incidence in Europe ;4-13/100 000 • Prevalence 41.76 / 100 000). • Men have a higher incidence & Black higher risk.
  • 12. Risk factors:Alcohol • The causative agent in nearly 50% • Major risk factor in 43%, either alone (34%) or in combination with ductal obstruction (9%). • More frequently in men (59%) than in women (28%). • Genetic variants in the CLDN2 gene loci have influence the risk ,higher in men than in women. • Alcohol increases the risk in a dose-dependent manner, doubles or trebles at a threshold of four or five drinks/ day. • The incidence in regular excess consumers is low (5–15%) • It is unclear whether there is truly any safe threshold of alcohol intake in relation to chronic pancreatitis. • Pathogenesis:chronic alcohol sensitises the acinar cell to injury by interfering with mechanisms protecting against stress induced by the endoplasmic reticulum.
  • 13. Risk factors:smoking • An independent risk facto. • The pooled risk estimate 2.5, dose-dependent&synergistic with alcohol. • Smoking as the strongest risk factor for progression from acute to chronic pancreatitis. • Nicotine induces oxidative stress in the pancreatic acini. • The nicotine metabolite 4-(methylnitrosamino)-1-(3- pyridyl)-1-butanone (NNK) has been implicated.
  • 14. Risk factors:genetics • Either by premature activation of trypsinogen or failure to inactivate trypsin during pancreatic inflammation. • Gain-of-function mutations in the cationic trypsin gene (PRSS1) lead to premature trypsinogen activation as the cause of hereditary pancreatitis. • Inheritance is autosomal-dominant with high penetrance, • Mutation in SPINK1 is not an independent risk factor but, it has disease-modifying properties implicated in the progression of recurrent acute pancreatitis to chronic pancreatitis& associated with tropical calcific pancreatitis. • Mutations in CFTR identified without pulmonary manifestations of CF& coinheritance with SPINK1 incr risk . • CTRC, CASR, CLDN2 on X ch, associated with CP. • Hereditary pancreatitis secondary to PRSS1 mutation is
  • 15. Risk factors:ductal obstruction • Ductal obstruction due to inflammatory strictures, benign tumours, or malignancies leads to chronic obstructive pancreatitis upstream from the obstruction. • Occasionally chronic pancreatitis might beconfined to the dorsal pancreas in patients with pancreas divisum, suggesting a causative role of ductal obstruction • A higher frequency of pancreas divisum has been noted in patients with CFTR mutation-associated pancreatitis
  • 16. Risk factors:idiopathic • Large proportion. • Before labelling idiopathic, thorough investigation is warranted. • Tropical pancreatitis, or fibrocalculous pancreatic, is a form the tropics, specially Southern India characterised by early-onset pain, large MPD calcification& rapid onset of ketosis-resistant diabetes. • Although genetic SPINK1, nutritional&inflaammatory factors have been implicated.
  • 17. Risk factors:pathogenesis • Protein-rich plugs form in the interlobular & intralobular ducts secondary to a failure in the compensatory increase of ductal bicarbonate secretion, which results in a viscous ductal microenvironment. • Ductal obstruction results in inflammation, which subsequently leads to pancreatic parenchymal fibrosis. • Ducts bstruction lead to pancreatic ductal hypertension with resultant hypoperfusion & ischaemic injury of acini. • ? A sentinel event of AP is a key element. • Pancreatic stellate cells can be activated (to form collagen &extracellular matrix, causing pancreatic parenchymal fibrosis) by chemokines as TGFβ ,PDGF released by pancreatic inflammation.
  • 18. Risk factors:Clinical features • Patients do not usually present with classic signs. • More often, patients present with recurrent clinically acute pancreatitis. • Over a varying time-interval (years - decades) progressive changes appear in the pancreas. • Initially such changes are visible only on endoscopic ultrasound. • Eventually, patients develop the clinical triad of abdominal pain, exocrine pancreatic insufficiency&diabetes. • Pain is often the over-riding symptom&present in up to 85%. • Exocrine insuff manifests as steatorrhoea&in severe cases, wt loss,malnutrition&fat-soluble vit deficiency.
  • 19. Risk factors:Clinical features • Endocrine insufficiency results in pancreatogenous diabetes, T3C DM to distinguish it from T1&T2DM. • Pain is usually post-prandial, epigastric with radiation to back, often with nausea /vomiting,partially relieved by sitting or leaning forward ,but the location, severity, character, intensity are highly variable.
  • 20. Risk factors:Clinical features • The mechanism of pain is poorly understood: • 1. Pancreatic ductal& parenchymal hypertension. • 2. Activation of intrapancreatic nociceptors, hypertrophy & inflammation of intrapancreatic nerves& abnormal pain processing in CNS. • 3.Intrapancreatic neural remodelling&similar changes in the viscerosensory cortex are key factors evidenced by poor correlation bet structural changes &severity of pain& pain persistence in total pancreatectomy.
  • 21. Risk factors:Clinical features • The clinical hallmark of pancreatic exocrine insufficiency is steatorrhoea that does not usually occur until pancreatic lipase output drops below 10–15% normal. • So maldigestion /steatorrhoea are of advanced stages. • The appearance of the stool is an unreliable predictor of steatorrhoea & 72 h faecal fat estimation, done when the patient is taking a diet restricted to 100 g of fat per day, is often required to establish diagnosis. • In the absence of other clinical / radiological features, isolated steatorrhoea is almost never secondary to CP.
  • 22. Risk factors:Clinical features • Most patients eventually develop T3CDM, but CP can occur with T1&T2DM. • A history of long-standing CP before the onset of diabetes is usually typical for diagnosis of T3CDM. • Patients are at a higher risk of hypoglycaemia due to concomitant loss of counter-regulatory hormones glucagon & pancreatic polypeptide. • Common complications:pseudocysts; CBD stricture; duodenal stenosis; pleural effusion; PVT; SPT with formation of gastric varices; pseudoaneurysm affecting the splenic, hepatic, gastroduodenal& pancreaticoduodenal arteries& pancreatic ascites • CP at a higher risk of pancreatic adenocan ,greatest for early-onset in patients with hereditary&tropical CP.
  • 23. Diagnosis • Often obvious in advanced cases. • In early stage diagnosis is challenging& often based on a combination of clinical, imaging &pancreatic funct testing. • In the absence of established diagnostic criteria, early diagnosis remains an elusive diagnosis.
  • 24. Diagnosis • Histology: • Fibrosis,parenchymal loss, lobular inflammation&ductal changes are key diagnostic histological features. • In late burntout CP, inflammation might be absent. • In autopsy pancreatic fibrosis is common in asymptomatic people &DM, so fibrosis alone is insufficient for diagnosis. • Sampling error is a major limitation for surgical and endoscopic biopsies &false-negative results. • There is also a risk of causing pancreatitis by EUS-FNA. • Overall, histology is rarely used to establish diagnosis.
  • 26. Diagnosis • CT & MRCP are reasonably sensitive for detection of advanced CP, but sensitivity is low. • IV secretin during MRCP increases sensitivity to detect ductal changes • With EUS, ERP no longer used for diagnosis. • The ductal changes noted on ERP (Cambridge classificationis), was considered the most reliable imaging test with sensitivity up to 90%.
  • 27. Diagnosis • The Rosemont EUS criteria for diagnosis combine ductal &parenchymal features; 4 categories: • Consistent,suggestive, indeterminate & healthy. • The Japanese EUS criteria include a category of early CP. • Sensitivities / specificities of > 80% to diagnose pancreatic fibrosis reported for EUS. • Concomitant presence of four or more EUS criteria has a sensitivity of up to 91%. • Pancreatic changes on EUS can also be seen in patients with no symptoms of pancreatic disease; so findings should always be interpreted in the appropriate clinical context & are rarely diagnostic of chronic pancreatitis in isolation.
  • 28. Diagnosis • Pancreatic function tests are classified as direct&indirect. • Direct pancreatic function tests have been phased out of clinical practice. • At some centres the secretin function test has been combined with EUS in which pancreatic fluid is collected endoscopically after secretin stimulation, allowing for a structural assessment of the pancreas at the same time, but not yet widely used.
  • 29. Diagnosis • Indirect pancreatic function tests include measurement of faecal elastase 1 & faecal fat. • A faecal elastase 1 > 100 μg/g of stool is used as a marker of pancreatic exocrine dysfunction. • The test result can be erroneously low with diarrhoea. • Faecal elastase 1 can be checked easily &not affected by concomitant panc enzyme replacement, so commonly used,but has low sensitivity& specificity in early disease & can have high false-positive with up to 10%. • 72 h faecal fat is cumbersome& not done at most centres. • Despite its limitations it is fairly reliable if done properly. • At present no single test in isolation is diagnostic. • Abns on EUS&PFTs in the absence of signs/ symptoms are not specific&should not be used for diagnosis.
  • 30. Management: Medical • Management of ; • Pain. • Exocrin einsufficiency. • Endocrine insufficiency. • Complications (biliary obstruction, bleeding, or malignancy).
  • 31. Management: Medical • Nutrition& lifestyle modification are key components. • Endoscopic/surgical interventions have a role in some. • Pain control is the most difficult challenge. • Long-term use of opioids is best avoided. • Adjunctive pain medication as TADs,gabapentin, pregabalin&SSRIs have been used either alone or in combination with opioids with variable results. • Tramadol have a similar efficacy with less side-effects. • Pan enzymes, octreotide, montelukast,antioxisants & allopurinol are not effective for pain. • Alcohol & smoking cessation can reduce pain. • Contributing factors looked for (pseudocysts, duod strictures& trt-related complications as opioid-induced bowel dysfunction or postop intra-abdominal adhesions).
  • 32. Management: endoscopic • The common clinical indications for endoscopic intervention: • 1.Intraductal stones in the region of the pancreatic head, • MPD stricture • Symptomatic pseudocyst. • Large stones usually need (ESWL). • ESWL + ERCP have not shown any added benefit. • Dominant strictures in MPD are managed by endoscopic pancreatic single stent long term. • EUS-CPN relieves pain in about 50% of patients, the effect lasts a maximum of a few weeks & not recommended for patients with painful CP without concomitant pan can.
  • 33. Management: endoscopic • In patients with pancreas divisum& recurrent pancreatitis, risks of minor papilla sphincterotomy (stenosis/ thermal duct injury) should be weighed against the potential prevention of recurrence, less helpful in established CP than recurrent AP. • Long-term pancreatic duct stenting induces morphological changes in MPD&parenchymal changes resembling CP& should be avoided in patients with pancreas divisum.
  • 34. Management: surgical • Surgical intervention is effective in carefully selected. • Common indications: • Poorly controlled pain • Duodenal, biliary &pancreatic duct obstruction; • Symptomatic pseudocysts • Suspicion of cancer. • Surgery classified into 3: • Drainage procedures • Partial pancreatic resection • Total pancreatectomy
  • 35. Management: pancreatic enzymes replacement • Treatment is often started at lower dose with 40 000–50 000 USP units of lipase with each meal & half that amount with snacks. • Lower doses of 25 000–40 000 units per meal might be effective& should be started at a low dose& titrated on the basis of clinical response. • Digestion calories should be equally divided 3-5 meals/day &enzyme pills distributed through the meal. • If there is no improvement in steatorrhoea at maximum doses,PPI+ alternative causes of diarrhoea explored. • The monitoring of serum fat-soluble vitamins A, D, and E &appropriate supplementation is important.
  • 36. Management: pancreatic endocrine insufficiency • Lifestyle modification is a key component of treatment. • Metformin is often the firs tline drug. • In time most patients need insulin therapy,but more prone to hypoglycaemia & need closely monitoring &insulin pump is often the safest & most effective. • The importance of smoking & alcohol abstinence, healthy eating habits& daily exercise is often underemphasised. • Referral to formal structured de-addiction programmes& a nutritionist should be considered when appropriate.
  • 39. Endoscopic Ultrasound Diffuse hypoechoic enlargement of pancreas. Fine needle aspirate of the pancreas was negative for tumor.
  • 40. ERCP There was a long segment of extrahepatic biliary stricture. The pancreatic duct was normal in size but irregular. Brushings, biopsies and bile aspirate were negative for tumor
  • 47. Abstract: • Chronic pancreatitis describes a wide spectrum of fibro-inflammatory disorders of the exocrine pancreas that includes calcifying, obstructive& steroid-responsive forms. • Epidemiology: incidence seems to be on the rise. Smoking, drinking alcohol& genetic predisposition are the major risk factors. • Management is focusing on pain management, the role of endoscopic & surgical intervention& the use of pancreatic enzyme-replacement therapy. • Management of patients is often challenging & necessitates a multidisciplinary approach.