PANCREATITIS
PRESENTED BY
ABHILASHA CHAUDHARY
 Elongated and tapered organ .
 A pale grey gland weighing about 60 grams
and about 12-15 cm long
 Situated in the epigastric and left
hypochondriac regions of the abdominal
cavity
 Parts
 Head -the widest right
part of the organ and lies
in the curve of the
duodenum
 Body- tapered left side
extends slightly upward
lies behind stomach.
 Tail- narrowed end part
lies infront of the kidney
and just reaches the
spleen.
FUNCTIONS
Endocrine functions
-Islet of langerhens
-Alphacells
glucagon(20%)
-Beta cells
insulin(75%)
-Delta cells
somatostatin
Exocrine functions
Pancreatic juice
-Amylase
-Lipase
-Trypsin
-Chymotrypsin
Carboxypeptidase
 Exocrine cells
 consists of a large number of lobules made up of
small acini, which consist of secretory cells.
 Each lobule is drained by a tiny duct and these
unite eventually to form the pancreatic duct.
 pancreatic duct joins the common bile duct to
form hepato pancreatic ampulla.
 The duodenal opening of the ampulla is
controlled by the hepatopancreatic sphincter of
the duodenal papilla.
 The function of the exocrine pancreas is to
produce pancreatic juice containing
enzymes,that digest carbohydrates, proteins
and fats.
 Pancreatic juice:
 Secreted by exocrine pancreas .
 Consists of:
 Water
 Mineral salts
 Enzymes:
 Amylase
 Lipase
 Inactivated enzyme precursor including
 Trypsinogen
 Chymotrypsinogen
 Functions
 Digestion of protein:
 Trypsinogen and chymotrypsinogen are inactive
enzyme precursors activated by enterokinase to
enzymes trypsin and chymotrypsin which convert
polypeptide to tripeptides and dipeptides.
 Digestion of carbohydrates
 Amylase converts polysaccharides(starches) to
disaccharides.
 Digestion of fats:
 Lipase converts fats to fatty acids and glycerol.to
aid the action of fats , bile salts emulsify fats.
 Control of secretions :
 When the partially digested contents of the
stomach reach the small intestine, two
hormones ,secretin and cholecystokinin are
produced by endocrine cells in the walls of
the duodenum and these hormones
stimulates the secretion of pancreatic juice.
 Endocrine functions
 consists of clusters of cells, known as the
pancreatic islets scattered throughout the
gland. they are directly secreted into the
blood stream and circulate throughout the
body.
 Alpha cells secrete glucagon
 Beta cells secret insulin
 Delta cells secrete somatostatin.
 Functions of insulin
 Reduces blood glucose levels
 Secretion is stimulated by increased blood
glucose level,e.g after eating a meal
 Functions of glucagon
 Increases blood glucose level.
 Secretion is stimulated by low blood glucose
levels and exercise, and decreased by
somatostatin and insulin.
 Functions of somatostatins
 Inhibits the secretion of insulin and glucagon in
addition to inhibiting the secretion of GH from
the anterior pituitary.
 Definition
 Pancreatitis is the inflammation of the
pancreas.
 pancreatitis is commonly described as
autodigestion of the pancreas.
TYPES
Acute
pancreatitis
Chronic
pancreatitis
 Acute pancreatitis
 It is an acute inflammatory process of the
pancreas.
 The degree of inflammation varies from mild
edema to severe hemorrhagic necrosis.
 Incidence
 Acute pancreatitis is most common in middle
aged men and women.
 It affects male and female equally.
Phospholipase fat necrosis
Elastase haemorrhage
Activates proteases which causes autodigestion of
pancreas,and activation of other proteolytic enzymes.
Trypsinogen CK trypsin
Activation of pancreatic enzymes
Etiological factors(Gallstone,ethanol,trauma etc)
 The pathophysiologic involvement of acute
pancreatitits ranges from edematous
pancreatitis (which is self limiting )to
necrotizing pancreatitis.
 Severe abdominal pain is predominanat
symptoms
 Pain located in upper quadrant and
midepigastrium
 Severe, deep piercing and continuous or
steady in nature
Hypotension
Nausea, vomiting
◦ Crackles
present over
lungs
◦ Illeus with
marked
abdominal
distension
Greys turner spots (bluish flank
discolouration)
Cullen’s sign(a bluish periumblical area)
 Tachycardia and jaundice
 Bowel sound may be decreased or absent
 Shock may be arise due to haemorrhage,
toxemia from activated enzymes.
 Hypovolemia as a result of fluid shift.
 Chronic pancreatitis is a continuous,
prolonged , inflammatory and fibrosing
process of the pancreas.
 Progressively destroyed as it is replaced with
fibrotic tissue.
 Strictures and calcification may also occur in
pancreas
 Pathophysiology
 The 2 major types are chronic obstructive
pancreatitits and chronic calcifying
pancreatitis.
 Toxic effect of alcohol causes obstruction of
duct with protein precipitates.the precipitates
block the pancreatic duct and eventually
calcify which is followed by fibrosis and
glandular atrophy. Pseudocyst and abscesses
commonly develop.
 Clinical manifestation
 Upper abdominal pain
 Losing weight without trying
 Oily, smelly stools (steatorrhea)
 Infections: In acute pancreatitis, the pancreas
is susceptible to bacteria that can cause
infections..
 Pseudocyst:Debris and fluid that can collect
in pockets of the pancreas. If this cyst-like
pocket ruptures, infection and bleeding can
result.
 Diabetes: Due to damage of the insulin
producing cells.
 Pancreatic abscess(cavity of pus within the
pancreas)
 Respiratory problems(pleural
effusion,atrelactasis,pneumonia)
 SIRS(systemic inflammatory response
syndrome)-vasodilation,hypotension,capillary
leakage,edema)
 Malnutrition: Due to lack of absorption.
 Pulmonary emboli, disseminated intravascular
coagulation.
 Primary test
 Serum amylase Increased (>200 U/L)
 Serum lipase Elevated
 Urinary amylase Elevated
 Secondary tests
 Blood glucose Hyperglycemia
 Serum calcium Hypocalcemia
 Serum triglyceride Hyperlipidemia
 Abdominal
ultrasonography
 Endoscopic
ultrasonography (EUS)
 Abdominal computed
tomography (CT)
scanning
 Endoscopic retrograde
cholangiopancreatogra
phy (ERCP)
 Collaborative care
 Objective of collaborative care for acute
pancreatitits include:
 Relief of pain
 Prevention or alleviation of shock
 Reduction of pancreatic secretions
 Control of fluid and electrolyte imbalances
 Prevention or treatment of infections
 Removal of the precipitating cause
 Conservative therapy
 Focused on supportive care
 Pain management(Iv
morphine,antispasmodic)
 Correction of hypovolemia using normal
saline and colloids.
 Use NG suction to reduce vomiting and
gastric distension
 Decrease stimulation of pancreas
 Avoidance of alcohol.
 Keep patient in NPO
 Oxygen for hypoxic patients those with acute
respiratory distress syndrome.
 Pharmacological therapy
 Morphine –relief of pain.
 Nitroglycerine or papaverine-relaxation of smooth
muscles and relief of pain.
 Antispasmodic(dicyclomine,propantheline
bromide)-decreased of vagal
stimulation,motility,pancreatic outflow.
 Carbonic anhydrase inhibitor (acetazolamide)
reduction in volume and bicarbonate concentration
of pancreatic secretions.
 Antacids – neutralizations of gastric
hydrochloride.
 Histamine(H2) receptor antagonists
ranitidine
 proton pump inhibitors (omeprazole)
-decrease in HCL and stimulates pancreatic
secretion
 Calcium :if hypocalcemia tetany occur
 Prophylactic broad spectrum antibiotic
 Pancreatic enzyme replacement.
 Nutritional management
 Diet: low in fat and high in protein and
carbohydrates
 Small frequent feeding
 Pancreatic enzyme supplementation with
meals
 Correct malabsorption of the fat-soluble
vitamins (A, D, E, K) and vitamin B12
 Medium-chain triglycerides in patients with
severe fat malabsorption (they are directly
absorbed by the small intestine without the
need for digestion).
 Surgical therapy
 Done in case of
 Abscess
 Severe peritonitis
 Acute pseudocyst.
 ERCP plus endoscopic sphincterotomy-
performed to remove duct obstruction - eg,
gallstone.
 Percutaneous drainage of pseudocyst.
 Choledochojejunostomy- Common bilde duct
is anastomosed into the jejunum where it
diverts bile around the ampulla of vater.
 Roux-en Y pancreatojejunostomy.
1.Acute pain related to distension of pancreas,
peritoneal irritation,obstruction of biliary
tract.
2. Risk for fluid volume deficit realted to
Excessive losses: vomiting, gastric
suctioning.
3. Imbalanced Nutrition: Less Than Body
Requirements related to Vomiting, decreased
oral intake; prescribed dietary
restrictions,Loss of digestive enzymes and
insulin .
 Research evidence
 Topic :Frequency and risk factors of recurrent
pain during refeeding in patients
with acute pancreatitis: a multivariate
multicentre prospective study of 116
patients.
 OBJECTIVES :
To assess the frequency and the risk factors of
pain relapse in patients with acute
pancreatitis.
 RESULTS:
 The cause of acute pancreatitis was biliary in
47% and alcohol misuse in 31%. During the
oral refeeding period, 21% of the patients had
pain relapse.
 CONCLUSION:
 Pain relapse occurred in one fifth of the
patients with acute pancreatitis during oral
refeeding and was more common in patients
with necrotic pancreatitis and with longer
periods of pain. The results of this study can
be used to predict high risk patients and are
a first step in the prevention of pain relapse.
 RESEARCH EVIDENCE
 TOPIC :Trends in the Use of Endoscopic
Retrograde Cholangiopancreatography for the
Management of Chronic Pancreatitis in the United
States.
 GOALS:
 The aim of this study was to characterize current
trends in the use of endoscopic retrograde
cholangiopancreatography (ERCP) in the United
States for patients hospitalized with
chronic pancreatitis.
 RESULTS:
 During the study period, 29,318 patients with
chronic pancreatitis (mean age 52 y, 57.2%
female) underwent ERCP during their
hospitalization.
 CONCLUSIONS:
 In the United States, ERCP has been an
important diagnostic and therapeutic tool for
chronic pancreatitis.
 REFERENCES
 BOOKS
 Smeltzer Suzanne C, Barebrenda G, Hinkle Janice
L, Cheever Kerry H. Textbook of medical surgical
nursing, 12th ed. Newdelhi: Lippincot wolter’s
kluwer; p.113-114(vol-1)
 Lewis Sharan mantik, Heitkemper Margaret
Mclean, Shannon Ruff Dirksen,Obrien Patrical,
Giddens Jean Foret, Bucher Linda. Medical
surgical nursing. 6th ed.Mosby; p.1052-56
 Best practices A guide to excellence in nursing
care. lippincott William and wikins. P.258-62.
 )
 JOURNALS
 Lévy P, Heresbach D, Pariente EA, Boruchowicz
A, Delcenserie R, Millat B, Moreau J, Le Bodic
L, de Calan L, Barthet M, Sauvanet .Frequency and
risk factors of recurrent pain during refeeding in
patients with acute pancreatitis: a multivariate
multicentre prospective study of 116 patients.
Gut;1997:20(1)

 Clark CJ, Fino NF, Clark N, Rosales A, Mishra
G, Pawa R. Trends in the Use of Endoscopic
Retrograde Cholangiopancreatography for the
Management of ChronicPancreatitis in the United
States. J Clin Gastroenterol;2016:50(5
ACUTE AND CHRONIC PANCREATITIS
ACUTE AND CHRONIC PANCREATITIS
ACUTE AND CHRONIC PANCREATITIS

ACUTE AND CHRONIC PANCREATITIS

  • 1.
  • 2.
     Elongated andtapered organ .  A pale grey gland weighing about 60 grams and about 12-15 cm long  Situated in the epigastric and left hypochondriac regions of the abdominal cavity
  • 3.
     Parts  Head-the widest right part of the organ and lies in the curve of the duodenum  Body- tapered left side extends slightly upward lies behind stomach.  Tail- narrowed end part lies infront of the kidney and just reaches the spleen.
  • 4.
    FUNCTIONS Endocrine functions -Islet oflangerhens -Alphacells glucagon(20%) -Beta cells insulin(75%) -Delta cells somatostatin Exocrine functions Pancreatic juice -Amylase -Lipase -Trypsin -Chymotrypsin Carboxypeptidase
  • 6.
     Exocrine cells consists of a large number of lobules made up of small acini, which consist of secretory cells.  Each lobule is drained by a tiny duct and these unite eventually to form the pancreatic duct.  pancreatic duct joins the common bile duct to form hepato pancreatic ampulla.  The duodenal opening of the ampulla is controlled by the hepatopancreatic sphincter of the duodenal papilla.
  • 8.
     The functionof the exocrine pancreas is to produce pancreatic juice containing enzymes,that digest carbohydrates, proteins and fats.
  • 9.
     Pancreatic juice: Secreted by exocrine pancreas .  Consists of:  Water  Mineral salts  Enzymes:  Amylase  Lipase  Inactivated enzyme precursor including  Trypsinogen  Chymotrypsinogen
  • 10.
     Functions  Digestionof protein:  Trypsinogen and chymotrypsinogen are inactive enzyme precursors activated by enterokinase to enzymes trypsin and chymotrypsin which convert polypeptide to tripeptides and dipeptides.  Digestion of carbohydrates  Amylase converts polysaccharides(starches) to disaccharides.  Digestion of fats:  Lipase converts fats to fatty acids and glycerol.to aid the action of fats , bile salts emulsify fats.
  • 11.
     Control ofsecretions :  When the partially digested contents of the stomach reach the small intestine, two hormones ,secretin and cholecystokinin are produced by endocrine cells in the walls of the duodenum and these hormones stimulates the secretion of pancreatic juice.
  • 12.
     Endocrine functions consists of clusters of cells, known as the pancreatic islets scattered throughout the gland. they are directly secreted into the blood stream and circulate throughout the body.  Alpha cells secrete glucagon  Beta cells secret insulin  Delta cells secrete somatostatin.
  • 13.
     Functions ofinsulin  Reduces blood glucose levels  Secretion is stimulated by increased blood glucose level,e.g after eating a meal  Functions of glucagon  Increases blood glucose level.  Secretion is stimulated by low blood glucose levels and exercise, and decreased by somatostatin and insulin.  Functions of somatostatins  Inhibits the secretion of insulin and glucagon in addition to inhibiting the secretion of GH from the anterior pituitary.
  • 14.
     Definition  Pancreatitisis the inflammation of the pancreas.  pancreatitis is commonly described as autodigestion of the pancreas.
  • 15.
  • 16.
     Acute pancreatitis It is an acute inflammatory process of the pancreas.  The degree of inflammation varies from mild edema to severe hemorrhagic necrosis.
  • 17.
     Incidence  Acutepancreatitis is most common in middle aged men and women.  It affects male and female equally.
  • 20.
    Phospholipase fat necrosis Elastasehaemorrhage Activates proteases which causes autodigestion of pancreas,and activation of other proteolytic enzymes. Trypsinogen CK trypsin Activation of pancreatic enzymes Etiological factors(Gallstone,ethanol,trauma etc)
  • 21.
     The pathophysiologicinvolvement of acute pancreatitits ranges from edematous pancreatitis (which is self limiting )to necrotizing pancreatitis.
  • 22.
     Severe abdominalpain is predominanat symptoms  Pain located in upper quadrant and midepigastrium  Severe, deep piercing and continuous or steady in nature
  • 23.
  • 24.
    ◦ Crackles present over lungs ◦Illeus with marked abdominal distension
  • 25.
    Greys turner spots(bluish flank discolouration) Cullen’s sign(a bluish periumblical area)
  • 26.
     Tachycardia andjaundice  Bowel sound may be decreased or absent  Shock may be arise due to haemorrhage, toxemia from activated enzymes.  Hypovolemia as a result of fluid shift.
  • 27.
     Chronic pancreatitisis a continuous, prolonged , inflammatory and fibrosing process of the pancreas.  Progressively destroyed as it is replaced with fibrotic tissue.  Strictures and calcification may also occur in pancreas
  • 29.
     Pathophysiology  The2 major types are chronic obstructive pancreatitits and chronic calcifying pancreatitis.
  • 30.
     Toxic effectof alcohol causes obstruction of duct with protein precipitates.the precipitates block the pancreatic duct and eventually calcify which is followed by fibrosis and glandular atrophy. Pseudocyst and abscesses commonly develop.
  • 31.
     Clinical manifestation Upper abdominal pain  Losing weight without trying  Oily, smelly stools (steatorrhea)
  • 32.
     Infections: Inacute pancreatitis, the pancreas is susceptible to bacteria that can cause infections..  Pseudocyst:Debris and fluid that can collect in pockets of the pancreas. If this cyst-like pocket ruptures, infection and bleeding can result.  Diabetes: Due to damage of the insulin producing cells.
  • 33.
     Pancreatic abscess(cavityof pus within the pancreas)  Respiratory problems(pleural effusion,atrelactasis,pneumonia)  SIRS(systemic inflammatory response syndrome)-vasodilation,hypotension,capillary leakage,edema)  Malnutrition: Due to lack of absorption.  Pulmonary emboli, disseminated intravascular coagulation.
  • 34.
     Primary test Serum amylase Increased (>200 U/L)  Serum lipase Elevated  Urinary amylase Elevated  Secondary tests  Blood glucose Hyperglycemia  Serum calcium Hypocalcemia  Serum triglyceride Hyperlipidemia
  • 35.
  • 36.
     Abdominal computed tomography(CT) scanning  Endoscopic retrograde cholangiopancreatogra phy (ERCP)
  • 37.
     Collaborative care Objective of collaborative care for acute pancreatitits include:  Relief of pain  Prevention or alleviation of shock  Reduction of pancreatic secretions  Control of fluid and electrolyte imbalances  Prevention or treatment of infections  Removal of the precipitating cause
  • 38.
     Conservative therapy Focused on supportive care  Pain management(Iv morphine,antispasmodic)  Correction of hypovolemia using normal saline and colloids.  Use NG suction to reduce vomiting and gastric distension  Decrease stimulation of pancreas  Avoidance of alcohol.  Keep patient in NPO
  • 39.
     Oxygen forhypoxic patients those with acute respiratory distress syndrome.
  • 40.
     Pharmacological therapy Morphine –relief of pain.  Nitroglycerine or papaverine-relaxation of smooth muscles and relief of pain.  Antispasmodic(dicyclomine,propantheline bromide)-decreased of vagal stimulation,motility,pancreatic outflow.  Carbonic anhydrase inhibitor (acetazolamide) reduction in volume and bicarbonate concentration of pancreatic secretions.
  • 41.
     Antacids –neutralizations of gastric hydrochloride.  Histamine(H2) receptor antagonists ranitidine  proton pump inhibitors (omeprazole) -decrease in HCL and stimulates pancreatic secretion
  • 42.
     Calcium :ifhypocalcemia tetany occur  Prophylactic broad spectrum antibiotic  Pancreatic enzyme replacement.
  • 43.
     Nutritional management Diet: low in fat and high in protein and carbohydrates  Small frequent feeding  Pancreatic enzyme supplementation with meals  Correct malabsorption of the fat-soluble vitamins (A, D, E, K) and vitamin B12
  • 44.
     Medium-chain triglyceridesin patients with severe fat malabsorption (they are directly absorbed by the small intestine without the need for digestion).
  • 45.
     Surgical therapy Done in case of  Abscess  Severe peritonitis  Acute pseudocyst.
  • 46.
     ERCP plusendoscopic sphincterotomy- performed to remove duct obstruction - eg, gallstone.
  • 47.
  • 48.
     Choledochojejunostomy- Commonbilde duct is anastomosed into the jejunum where it diverts bile around the ampulla of vater.
  • 49.
     Roux-en Ypancreatojejunostomy.
  • 50.
    1.Acute pain relatedto distension of pancreas, peritoneal irritation,obstruction of biliary tract. 2. Risk for fluid volume deficit realted to Excessive losses: vomiting, gastric suctioning.
  • 51.
    3. Imbalanced Nutrition:Less Than Body Requirements related to Vomiting, decreased oral intake; prescribed dietary restrictions,Loss of digestive enzymes and insulin .
  • 52.
     Research evidence Topic :Frequency and risk factors of recurrent pain during refeeding in patients with acute pancreatitis: a multivariate multicentre prospective study of 116 patients.  OBJECTIVES : To assess the frequency and the risk factors of pain relapse in patients with acute pancreatitis.
  • 53.
     RESULTS:  Thecause of acute pancreatitis was biliary in 47% and alcohol misuse in 31%. During the oral refeeding period, 21% of the patients had pain relapse.
  • 54.
     CONCLUSION:  Painrelapse occurred in one fifth of the patients with acute pancreatitis during oral refeeding and was more common in patients with necrotic pancreatitis and with longer periods of pain. The results of this study can be used to predict high risk patients and are a first step in the prevention of pain relapse.
  • 55.
     RESEARCH EVIDENCE TOPIC :Trends in the Use of Endoscopic Retrograde Cholangiopancreatography for the Management of Chronic Pancreatitis in the United States.  GOALS:  The aim of this study was to characterize current trends in the use of endoscopic retrograde cholangiopancreatography (ERCP) in the United States for patients hospitalized with chronic pancreatitis.
  • 56.
     RESULTS:  Duringthe study period, 29,318 patients with chronic pancreatitis (mean age 52 y, 57.2% female) underwent ERCP during their hospitalization.  CONCLUSIONS:  In the United States, ERCP has been an important diagnostic and therapeutic tool for chronic pancreatitis.
  • 57.
     REFERENCES  BOOKS Smeltzer Suzanne C, Barebrenda G, Hinkle Janice L, Cheever Kerry H. Textbook of medical surgical nursing, 12th ed. Newdelhi: Lippincot wolter’s kluwer; p.113-114(vol-1)  Lewis Sharan mantik, Heitkemper Margaret Mclean, Shannon Ruff Dirksen,Obrien Patrical, Giddens Jean Foret, Bucher Linda. Medical surgical nursing. 6th ed.Mosby; p.1052-56  Best practices A guide to excellence in nursing care. lippincott William and wikins. P.258-62.  )
  • 58.
     JOURNALS  LévyP, Heresbach D, Pariente EA, Boruchowicz A, Delcenserie R, Millat B, Moreau J, Le Bodic L, de Calan L, Barthet M, Sauvanet .Frequency and risk factors of recurrent pain during refeeding in patients with acute pancreatitis: a multivariate multicentre prospective study of 116 patients. Gut;1997:20(1)   Clark CJ, Fino NF, Clark N, Rosales A, Mishra G, Pawa R. Trends in the Use of Endoscopic Retrograde Cholangiopancreatography for the Management of ChronicPancreatitis in the United States. J Clin Gastroenterol;2016:50(5