Chronic_pancreatitis.ppt
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Chronic pancreatitis
Ermias D (MD)
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Definition
Irreversible damage to the pancreas with
histologic evidence of inflammation,
fibrosis, and destruction of exocrine
(acinar) and endocrine (islets of
angerhans) tissue
Etiologic classification ! clinicall" useful
! #istologic ! accessibili" of tissue
! Imaging ! late morphologic changes
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prevalence
$utops" reports ! %&%'* overestimates
+etrospective studies ! -./%%,%%%
0rospective data
! among alcoholics ! 1&2."r./%%,%%%3
! overall prevalence 24&'./%%,%%%
5apan overall prevalence ! 21&./%%,%%%3
! M67 8&6/
$lcohol abuse ! 2. of causes Mortalit" &9: age matched control
$dvanced age, alcoholism and smo;ing are
poor prognostic conditions
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pathoph"siolog"
Incompletel" understood
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Ductal obstruction h"pothesis
Chronic alcohol use acinar and ductal cell
protein rich pancreatic =uice, low in volume and #C>
formation of protein precipitates ! plug
calcification of ppt ! ductal stone formation ductule obstruction
parench"mal damage
0ancreatic ductal stone are seen in alcoholic, tropical, hereditar",idiopathic
#istologic changes of C0 ma" be seen with out ductal obstruction
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?oxic metabolic h"pothesis
(alcohol)Direct in=urious effect on acinar and ductalcells
Increased membrane lipid peroxidation (oxidative
stress),free radical production Increase acinar cell sensitivit" to pathogenic
stimuli
@timulate CCA production (duodenal I cells)!
activation of proinflammator" transcription factors $ctivation of pancreatic stellate cells (alcohol,
c"to;ines)! produce proteins of extracellular matrix
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Becrosis fibrosis h"pothesis
+epeated episodes of acute pancreatitis withcellular necrosis or apoptosis, healing replacesnecrotic tissue with fibrosis
Evidence from natural histor" studies more severeand freuent attac;s
More evidence from hereditar" pancreatitis and
animal models
ut some have evidence of chronic pancreatitis
at time of first clinical acute attac;
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C7?+! c"stic fibrosis transmembrane conductance regulator
! C"stic fibrosis is ass& with abnormalities of #C>secretion, ductal dilatation, ppt formation, pancreaticatroph"
! @een in %* of idiopathic C0, not common in alcoholicC0
0+@@/! cationic tr"psinogen gene
! >nce tr"psinogen is activated to tr"psin, becomesresistant to inactivation and activate other proen"mes
leading to episodes of acute pancreatitis
! li;e necrosis fibrosis theor"
@0IBA/ serine protease inhibitor Aaal t"pe /! @een in pediatric IC0, hereditar" 0, ?03 but not in chronic
alcoholic pancreatitis
! ?r"psin inhibitor, mimic tr"psinogen gene
Fenetic forms
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Disease modif"ing genes
0ol"morphisms that modulate immune
response
C"to;ines !
! transforming growth factors G, H, interleu;in
/%, interferon gamma
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Etiologic factors ass&
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?+>0IC$ 0$BC+E$?I?I@
$frica, India, rail3 with in % latitude $ disease of earl" childhood and "outh
J -%* before age of '%"rs
0revalence in endemic areas6 / in %%1%%
$bdominal pain, malnutrition, exocrine andendocrine insufficienc"
0ancreatic caliculi ! -%*
7ibrocalculous pancreatic diabetes, tropicalcalcific pancreatitis
%* @0IBA/ gene mutation (B'@)
Knclear environmental trigger ! 0EM, Cassava
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$utoimmune pancreatitis
Confusing and evolving nomenclature
* of C0, more in males, middle age
/2 ! %* ass&
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Diabetes mellitus
/* of DM from C0
In DM pancreas is smaller,! abnormal duct in '%%* ,
! abnormal pancreatic fn in '%%*
Insulin is a trophic factor for exocrine fn of the pancreas
Insulin def L microangiopath" of DM lead to pancreaticdamage
DM and C0 cause effect r.n is not clear
Increased ris; of h"pogl"cemia due to glucagon
deficienc" when insulin therap" is initiated Flucagon li;e peptide infusion increases endogenous
insulin
Flucocorticoid tx for autoimmune cp reverses ass& DM
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Idiopathic C0 /%%* of acute pancreatitis
Earl" onset! 2%"r mean age, m8f
-9* pain
Calcification, exocrine or endocine insufficienc"
develop slowl" over time ! 2, 29 24& "rs C7?+, @0IBA/ genes
ate onset
0ain is less freuent '*4* $ge of onset 9"rs, m8f
Exocrine and endocrine insuf& Kpto '9 and '/*,
in /9&- and //&-"rs3 -%* calcification
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Clinical features
$bdominal pain
!$cute pancreatic inflammation
! Increased intrapancreatic pressure
!$lterations in pancreatic nerves
@teatorrhea ! lipase secretion /%*
DM
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diagnosis
Bo single test is adeuate
?ests for function
?ests for structure oth are more accurate in advanced
disease
Indicate large reserve functionall", latestructural changes
ig duct vs small duct disease
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?ests of function! hormone stimulation! @ecretin. secretin CCA test
! 7ecal elastase! 7ecal ch"motr"psin! @erum tr"psinogen (tr"psin)! 7ecal fat
! lood glucose
?ests of structure! Endoscopic K@
! E+C0! M+I.M+C0
! C?!$bdominal K@
! 0lain abdominal film
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+outine lab& tests
@erum am"lase and lipase
! Ma" be elevated in acute exacerbations
!$lso found increased in pseudoc"st, ductal
stricture, internal pancreatic fistula
>ther chemistr" and electrol"tes depend
on associated conditions
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Classics of Chronic pancreatitis
0ancreatic calcification @teatorrhea
Diabetes mellitus
7ound in less than a third of pts with C0
abnormal secretin stimulations test when
J9% * affected @erum tr"psinogen 2%ng.ml, fecal
elastase /%%mcg.mg stool severe
exocrine insuf&
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K@ or C? grading s"stem
Bormal ! no abnormalit" on good ualit" stud"
Euivocal ! mild parench"mal duct dilatation (2'mm)! gland enlargement 2 fold
Mild !moderate Lduct dilatation J'mm,N duct irregularit",N cavit" /%mm,N parench"mal heterogenit",N increased echo of duct wall,N irregular head and bod",N focal parench"mal necrosis
@evere Lcavit" J/%mm,N intraductal filling defects,N caliculi. pancreatic calcification,N ductal obstruction.stricture,N severe ductal dilatation or irregularit",N contiguous organ invasion
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li ti
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complications Cobalamin malabsorption
! Excess binding b" cobalamin binding proteins other
than intrinsic factor which were degraded b"pancreatic en"mes DM! but end organ damages of DM and DA$ are rare Bon DM retinopath"(peripheral) due to Oit $ and Pn defc& 0leural, peritoneal and pericardial effusionswith high
am"lase FI bleeding! 0KD, gastritis, pseudoc"st, varies (@Othrombosis)
Cholestasis, icterus, cholangitis, biliar" cirrhosis 7istula! internal or external
@ubcutaneous fat necrosis! tender red nodules on theshins
0seudoc"st, obstruction 0ancreatic carcinoma ! '* life time ris; Barcotic addiction
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treatment $im 0ain control and mx of maldigestion
0ain
!$void alcohol
! ow fat meals
!$ntipain ! narcotics (addiction)! @urgical pain control +esection (local -*) ! pancreatic insufficienc"
@planchinectom", celiac ganglionectom", nerve bloc;
! Endoscopic tx
@phinctorotom", dilatation of strictures, caliculi removal, duct
stenting
! Cpx ! acute pancreatitis, abscess, ductal damage, death
! 0ancreatic en"mes
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$bdominal pain !
+.o ddx ! K@ (no mass)!
secretin test (decreased #C> and volume)! 'w; pancreatic en"me!
('1tablets at meals and at bed time)!
minimal change C0 pt get relief of pain ! if not, E+C0.EK@ !
pseudoc"st, obstruction, dilated duct !
surger", octreotide! If Bo response
subtotal pancreatic resection
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?x of maldigestion 0ancreatic en"me replacement
! 2 enteric coated or 1 conventional tablets with meals! ad=uvants with conventional tablets ! #2 bloc;ers, 00I,
Ba bicarbonate,! Ca carbonate and Mg ># ma" even ppt steatorrhea
@teatorrhea can be abolished if /% * of normallipase amount can be delivered to the duodenumat the right time
imitations! ipase is inactivated b" gastric acid,
! food and en"me empt"ing from the stomach isdifferent,
! variable en"matic activit" of the preparation,! high potenc" prep& $nd colonic stricture reports