Acute &

Chronic
pancreatitis
‫ھذه اﻟﻣﺣﺎﺿرة ھﻲ ﺗﻛرﯾم ﻟﻛل ﻣن ﯾﻌﻣل وﻻ‬
‫ﻟﻛل اﯾﺎدي ﺗدﻓﻌﻧﺎ‬،‫ﻟﻛل ﻣن ﯾﻌﻣل ﺑﺎﻟﺧﻔﺎء‬،‫ﯾﻛرّ م‬
‫ﻣن ظﮭورﻧﺎ ﻻ ﻧرى وﺟوه اﺻﺣﺎﺑﮭﺎ‬

Objectives:

● Describe the definition, epidemiology,

pathogenesis, morphology, and clinical findings
of acute and chronic pancreatitis

Content Explanation Notes Important

 Pancreatitis

overview
https://youtu.be/ux45pMrtsy0

Pancreatitis: a group of disorders characterized by

inflammation of the pancreas, divided into acute
and chronic forms.

Chronic pancreatitis:
Acute pancreatitis: glands
irreversible destruction of
can return to normal if
exocrine pancreatic
underlying cause of the
parenchyma. permanent,
pancreatitis is removed.
main features : fibrosis,
Can resolve completely by
ducts dilation and
regeneration of acini
dystrophic calcification *

*Bridge to Histology: ‫طﯾب ﺣﻧﺎ ﺧذﻧﺎ ﻓﻲ اﻟﮭﺳﺗوﻟوﺟﻲ ان‬

The pancreases formed of two main parts
(Stroma) , (Paranchyma)it’s a mixed gland
Paranchyma ‫ﺣﻧﺎ ﻛﻼﻣﻧﺎ ﻋن ال‬
Two glands:
Exocrine: acini & duct produce DIGESTIVE Enz
Endocine:islets of langerhans produce hermons
‫اﻟﻣﮭم واﻟﻣﺗﺄﺛر ھﻲ اﻷﻛﺳو ﻻﻧﮭﺎ ھﻲ ﺗﻧﺗﺞ اﻷﻧزﯾﻣﺎت اﻟﮭﺎﺿﻣﺔ‬
 Acute Pancreatitis osmosis overview

٧ ‫ﻓﯾﮫ ﻣﻠﺧص ﻟﮫ ﺑﺳﻼﯾد‬

Definition Is a necro-inflammatory disease that is characterized by
infiltration of the pancreas by inflammatory cells and
destruction of the pancreatic exocrine cells.
Reversible condition.

Epidemiology The incidence in Western countries is 10 to 20 per 100,000

people. 80% of cases in Western countries are associated with
one of two conditions:
1- biliary tract disease (stones) 2- alcoholism.
Gallstones are present in 35% to 60%.
The male-to-female ratio is 1 : 3 in the group with biliary
tract disease and 6 : 1 in those with alcoholism
Alcoholism more in males, Stones more in females
Etiologic Factors :
10% to 20% of cases of acute pancreatitis are idiopathic pancreatitis

Metabolic 1- Alcoholism 2- Hyperlipoproteinemia(increase lipid in serum)

3- Hypercalcemia 4- Drugs (e.g., azathioprine)

Genetic Mutations in:

hereditary ● the cationic trypsinogen(PRSS1) autosomal dominant
pancreatitis ● trypsin inhibitor (SPINK1) genes premature activation of
trypsinogen into trypsin
or proteins that regulate calcium metabolism

Mechanical 1- Gallstones obstruction leads to accumulation of pancreatic enzymes

2- Trauma sharp trauma mainly most in children « seat belt »
3- Parasites: e.g. Ascaris lumbricoides and Clonorchis
sinensis
4- Iatrogenic injury: I. Operative injury
II. Endoscopic procedures with dye injection

Vascular 1-Shock
decreased 2-Atheroembolism
blood supply 3- Vasculitis (Polyarteritis nodosa )

Infectious Mumps, Coxsackievirus, Mycoplasma pneumoniae

 Acute Pancreatitis

Pathogenesis: Autodigestion of the pancreatic substance by inappropriately

activated pancreatic enzymes.
due to stone or
‫ﻣن اﺣد اﻷﺳﺑﺎب‬ tumor in the duct
‫ وﺟود‬stones
‫ ﻣﻣﻛن ﺗﺳوي‬block
★ seat belt trauma
‫ﺑﺎﻟﺗﺎﻟﻲ‬ most common
The fluid cause in normal
thickness will children who don’t
have hereditary
increase which abnormalities.
lead to edema seat belt trauma causes
then ischemia pancreatitis in children because it
then cell injury will produce pressure in the
upper gastrium then direct
injury to the pancreas.

★ There’s a fascia
around the
pancreas, so
there’s a limited (within the pancreatic cells)

space (any edema

or ↑ fluid in the
pancreatic tissue)
lead to ↓ blood
supply.

Mechanisms protect the pancreas from enzymatic self- digestion:

Most proenzymes are Acinar and ductal cells
activated by trypsin, which secrete trypsin inhibitors,
Most digestive enzymes are including serine protease
itself is activated by
synthesized as inactive inhibitor Kazal type l
duodenal enteropeptidase
proenzymes (zymogens), (SPINK1), which further
(enterokinase) in the small
which are packaged within limit intrapancreatic trypsin
bowel.
secretory granules. activity. If there’s deficiency or
Bridge to physiology:
Trypsin is activated either by mutation in the gene this will lead to
Enteropeptidase or another trypsin
hereditary pancreatitis.

Alcohol effects on pancreas:

● increases pancreatic exocrine secretion and contraction of the sphincter
of Oddi so there will be obstruction.
● Direct toxic effects on acinar cells with induction of oxidative stress in
acinar cells.
● Stimulate release of cytokines from acinar cells. These cytokines will induce the
neutrophils and inflammatory cells to come to the area so there will be acute pancreatitis.
 Acute Pancreatitis

Fat necrosis in the

There is
peripancreatic fat
Morphology

edema in
Hemorrhage in the the
pancreas.
Gross

head of the pancreas

Fat necrosis results from enzymatic destruction of fat cells.

The released fatty acids combine with calcium to form
insoluble salts that precipitate in situ (appear as foci of
yellow-white, chalky material). Calcium that binds to fat came from
blood so there will be hypocalcemia in the serum.

The morphology of acute pancreatitis ranges from

inflammation and edema to severe extensive necrosis and
Histopathologic

hemorrhage.
Morphology

The basic alterations are:

1- An acute inflammatory reaction with edema
2- Necrosis of peripancreatic fat by lipolytic enzymes
3- Proteolytic destruction of pancreatic parenchyma.
4- As as a result of tissue destruction
there will be Destruction of blood
vessels with subsequent
interstitial hemorrhage.

Bridge to biochemistry:
Lipase enzyme digest fats resulting 2-monoacylglycerols and fatty acids

This is one of the acute emergency condition

Features
Clinical

● Fever, nausea, and vomiting

● Severe, boring (knife-like) midepigastric pain (the
cardinal manifestation of acute pancreatitis) with
radiation into the back because it’s a retroperitoneal organ
● Hypovolemic shock in severe cases
● Tetany: calcium is used up in binding to fatty acid.
 Acute Pancreatitis

● Marked elevation of serum amylase levels during the first

Laboratory Findings

24 hours, followed within 72 to 96 hours by a rising serum

lipase level. Non-specific as it is secreted from the pancreas and salivary
glands
● Serum lipase: more specific because it’s only secreted from the
pancreas and lasts longer than amylase in acute pancreatitis;
excellent screen for acute pancreatitis.
● Release of lipases and phospholipases produce chalky areas
of fat necrosis, with precipitation of calcium that lowers
serum calcium (the worse the inflammation, the lower serum
calcium level which predict a worse prognosis).
Manage

The key to the management is "resting" the pancreas by total

ment

restriction of food and fluids and by supportive therapy

(intravenous fluids to replace the fluid supply he/she needs and nasogastric
suction from the stomach and intestine). They don’t need antibiotics.

● —Most patients recover fully

Prognosis

● About 5% die from:

1- Shock (during the first week of illness).
2- Acute respiratory distress syndrome. Usually fatal.
3- Acute renal failure.

1- Pancreatic necrosis (Systemic signs occur earlier than usual with

higher fever than usual; sinus tachycardia and greater degree of
neutrophilic leukocytosis and peripancreatic infections.
Complications

2- Pancreatic abscess (sterile) It means there’s no bacteria.

3- Pancreatic pseudocyst (due to liquefied necrosis area becomes
surrounded by granulation tissue, forming a cystic mass with no
epithelial lining)
4- Others:
a. hyperglycaemia ↑ glucose (destruction of β-islet cells)
b. hypocalcaemia and 2ry tetany due to Ca binding to FA
c. peritonitis If it’s severe, lipases and hydrolysis enzymes will be released in the
peritoneum leading to chemical pancreatitis.
 ‫‪Sumup of Acute pancreatitis:‬‬
‫‪Acute pancreatitis:‬‬
‫‪ reversible‬اھم ﺷﺊ ﻧﻌرﻓﮫ اﻧﮫ‬
‫‪ :).happy ending‬ﻓﻲ ﺣل ﻟﻠﺑﻧﻛرﯾﺎﺗﺎﯾﺗس‬
‫طﯾب ﺧﻠﻧﺎ ﻧﻌرف ﺷوي ﻋﻧﮫ‬
‫ھﻲ ﺗﺗﺄﺛر ﻷﻧﮭﺎ ﺗﻧﺗﺞ اﻷﻧزﯾﻣﺎت اﻟﮭﺎﺿﻣﺔ ﻟﻛن ﺑﺧﻠل ﻣﻣﻛن ﺗﻧﻌﻛس اﻵﯾﺔ وﯾﺑدأ اﻟﺑﻧﻛرﯾﺎس ﺑﮭﺿم ﻧﻔﺳﮫ ‪Exocrine gland‬‬
‫إﯾش اﻷﺳﺑﺎب ؟‬
‫‪ alcohol, gallstones, trauma, (PRSSA1, SPINK1) gene mutations‬اﻷﺳﺑﺎب ﻛﺛﯾرة ﻣﻣﻛن‬
‫ھذوﻟﻲ اھم اﻷﺳﺑﺎب وﻟﻸﺳف اﺣﯾﺎﻧﺎ ً ﯾﻛون اﻟﺳﺑب ﻣﺟﮭول ﺑس ﺑﻧﺳب ﺿﺋﯾﻠﺔ‬
‫طﯾب ھل ﻣﻌﻘول ان اﻟﺟﺳم أﺻﻼً ﯾﺧﻠﻲ أﻣر ﯾﺣﺻل ﺑﺳﮭوﻟﺔ وﻻ ﻋﻧده دﻓﺎﻋﺎت؟‬
‫اﻟﺟﺳم ﺑﯾداﻓﻊ ﻋن ﻧﻔﺳﮫ ﻛﯾف‬
‫أوﻻً‬
‫ھذول اﻷﻧزﯾﻣﺎت اﻟﮭﺎﺿﻣﺔ ﻣﺎرح ﺗﻛون ‪ ٢٤‬ﺳﺎﻋﺔ ﺗﺷﺗﻐل وﺗﮭﺿم ﻻ ﺑس ﻟﻣﺎ ﯾﺣﺗﺎﺟﮭﺎ اﻟﺟﺳم ﻓﺗﻛون ﺑﺣﺎﻟﺔ ﺧﻣول )‪(zymogens‬‬
‫ﺛﺎﻧﯾﺎ ً‪:‬‬
‫ﻟﻧﻔرض ان اﻟﺟﺳم ﯾﺣﺗﺎج اﻧﮫ ﯾﺑدأ ھﺿم اﻟﺣﯾن أﯾﺿﺎ ً ﻣب اي ﺷﻲ ﯾﺣﻔز ھذول اﻷﻧزﯾﻣﺎت اﻧﮭﺎ ﺗﺑدأ ھﺿم ﻻااا‬
‫‪ trypsin‬ﯾﺟﻲ ال‬
‫اﻟﻠﻲ ھو ﺑﻧﻔﺳﮫ ﯾﺣﺗﺎج ﺗﺣﻔﯾز أﻣﺎ ﻣن‬
‫‪enteropeptidase or other activated trypsin‬‬
‫ﺑﻌد ﻣﺎ ﯾﺗﺣﻔز ھو ﯾروح ﯾﺣﻔزھم ﻋﺷﺎن ﯾﺑدون ﺷﻐل‬
‫ﺛﺎﻟﺛﺎ ً‪:‬‬
‫اﻟﻌﻣل ﻻ ﯾﺧﻠو ﻣن اﻟﺧطﺄ‪ ،‬ﻓرﺿﺎ ً زادت ﻛﻣﯾﺔ ﻧﻔس اﻟﺧﻼﯾﺎ‬
‫ﺗﻧﺗﺞ أﻧزﯾم ﻣﺛﺑط )‪ (ductal and acinar‬اﻟﻠﻲ ھو )‪(trypsin inhibitor‬‬
‫ﯾﻣﻧﻊ اﻟﺗرﺑﺳن اﻧﮫ ﯾﺣﻔز اﻟﻣزﯾد ﻣن اﻷﻧزﯾﻣﺎت ﻓﺗوﻗف اﻟﻌﻣﻠﯾﺔ ھﻧﺎ وﺗﻧﺣل ھذي اﻟﻣﺷﻛﻠﺔ اﻟﺑﺳﯾطﺔ‬

‫طﯾب ﻟﻧﻔرض اﻵن أن ﺟﺎﻛم ﻣرﯾض ﯾﻌﺎﻧﻲ ﻣن‬

‫‪severe abdominal pain , fever, nausea , vomiting‬‬
‫و ﯾوم ﺗﻌرﻓون ﻋن اﻟﻣرﯾض اﻛﺛر ﯾﺗﺿﺢ اﻧﮫ ‪alcoholic‬‬
‫‪ abdominal pain‬ﻟﯾش ﻗﻠت‬
‫‪ mid epigastric pain‬وﻣﺎ ﻗﻠت‬
‫ﻻن اﻟدﻛﺗورة ﻗﺎﻟت ﻣﻣﻛن ﻧﺟﯾﺑﮫ ﺑﮭذي اﻟﺻﯾﻐﺔ ﻣﻊ أﻋراض‬
‫وﺗﺣددون ‪ +‬ﯾوم ﯾﺟﯾﻛم ﻣرﯾض ﻣﺎرح ﯾﻘوﻟﻛم اﻟﻣﻧطﻘﺔ ﺑﺎﻟﺿﺑط ﺑس ﯾﻘول ﺑطﻧﻲ‬
‫طﯾب اﻟﺣﯾن أول ﺷﻲ ﺗﺗرﻛون اﻟﻘﮭوة اﻟﻠﻲ ﺑﯾدﻛم وﺗﻘوﻣون ﻟﻠﺷﻐل 😂 ‪ +‬ﻣﺎ ﺗﻘدرون ﻣﺎ ﺗﻔﻛرون ب ﺑﻧﻛرﯾﺎﺗﺎﺗﯾس ﺑس ﯾﺑﯾﻠﻛم ﺗﺳوون‬
‫ﻓﺣوﺻﺎت ﻋﺷﺎن ﺗﺗﺄﻛدون‪،‬‬
‫‪ Fat necrosis , hemorrhage‬وش ﺷﻔﺗم ﺑﺎﻟﺑﻧﻛرﯾﺎس؟‬
‫‪ fat necrosis due to destruction of fat cells that released fatty acid combine with calcium‬ﻟﻠﺗوﺿﯾﺢ‬
‫ﻛﺎﻟﺳﯾوم؟ أي ﻛﺎﻟﺳﯾوم ﻷن طﺑﯾﻌﻲ ﯾﺗﺄﺛر وﻟو رﺟﻌﺗوا ﻟل‬
‫‪ Mutation of proteins that regulate calcium‬ﻓﯾﮫ ‪factors‬‬
‫ﻻ ﺗﻘوﻟوﻟﻲ ﺳﺣﺑﺗو ﻋﻠﯾﮭﺎ🌚 ﻣﺎ ﯾﺻﺣش ﯾﺎ ﺟﻣﺎﻋﺔ‬
‫طﯾب وش ﺷﻔﺗم ﺑﺎﻟﮭﺳﺗوﻟوﺟﻲ ؟‬
‫‪acute inflammatory reaction with edema, fat necrosis, destruction of‬‬
‫‪pancreatic Parenchyma and blood vessels destruction‬‬

‫؟‪ laboratory test‬ﺳوﯾﺗوﻟﮫ‬

‫‪Marked elevation of amylase enzyme + lipase enzyme why lipase? Fat necrosis‬‬
‫ﯾﺗﻼﻗون اﻻﻣﺎﯾﻠﯾز ﻣرﺗﻔﻊ ﺑس ﻷول ‪ ٢٤‬ﺳﺎﻋﺔ ف ﻣﺎھو ﻣﺣدد اﻧﮫ اﻛﯾوت ﺑﻧﻛرﯾﺎﺗﺎﯾﺗس‬
‫‪ indicator of acute pancreatitis‬ﻻﻧﮫ ﯾﺟﻠس ﻓﺗرة ﯾطول ف ھو ‪ lipase‬ال‬
‫ﺑﯾﻛون ﻓﯾﮫ ﻛﺎﻟﺳﯾوم زي ﻣﺎ ﻋرﻓﻧﺎ ﻗﺑل ﻟﯾش ﻛﻠﻣﺎ ﻛﺎﻧت ﻛﻣﯾﺔ اﻟﻛﺎﻟﺳﯾوم أﻗل ﻛﺎﻧت اﻟﺣﺎﻟﺔ أﺳوا‬
‫ﻛﯾف ﺗﺗﻌﺎﻣل ﻣﻌﺎه؟ ‪ acute pancreatitis‬ﻋرﻓﺗم اﻟﺣﯾن ان اﻟﻣرﯾض ﻋﻧده‬
‫اھم ﺷﺊ اﻧك ﺗﻘول ﻟﻠﻣرﯾض ﯾرﺗﺎح وﯾﺗرك اﻟﻣﺳﺑب اﻟرﺋﯾس ﻟو ﻛﺣول ﯾﺗرﻛﮭﺎ‬
‫ﯾﻛﺛرﻣوﯾﺔ ‪gallstone‬‬
‫‪supporting therapy‬‬
 Chronic pancreatitis osmosis overview

Chronic Chronic pancreatitis is defined as prolonged

inflammation of the pancreas with
Pancreatitis
irreversible destruction of exocrine
parenchyma, and, in the late stages,
associated with pancreatic insufficiency,
steatorrhea, diabetes due to destruction of
islet- beta cells, pancreatic calcification, and
fibrosis.

Epidemiology ● The prevalence of chronic pancreatitis

ranges between 0.04% and 5%
● Occurs in men more often than women
● Most affected patients are middle-aged
males

Chronic pancreatitis: Causes

➔ Majority idiopathic
➔ Known causes:
1. Alcohol abuse is the most common known cause (protein plugs form in
ducts and become calculi in the pancreatic duct)
2. Cystic fibrosis causes a thick secretion because there is no water
within the secretion is the most common cause in children. Germline
mutations in CFTR gene (cystic fibrosis transmembrane conductance
regulator)
3. Biliary tract disease: calculi or malformation
4. Malnutrition is the most common cause in developing countries
5. Autoimmune disorder
6. Long-standing obstruction of the pancreatic duct by calculi or
neoplasm.
 Chronic pancreatitis

1- Parenchymal fibrosis.
morphology pancreatitis is
characterised
2- Reduced number and size of acini with relative
Chronic

sparing of the islets of langerhans

by:

3- Variable dilation of pancreatic ducts

4- Calcium deposition

● Gland is hard pancreas normally is a soft gland

● Sometimes with extremely dilated ducts and
Gross

visible calcification

1- Extensive fibrosis and atrophy

has left only residual islets and ducts.
Microscopic
morphology

2- Chronic inflammatory cells

3- few acinar

1- Dilated ducts.
2- Inspissated eosinophilic ductal
concretions in case of alcoholic
chronic pancreatitis.
‫ﻛﻧﮭﺎ رﺟﺎل ﻋﻧده ﻟﺣﯾﺔ‬

1- Silent.
2- Severe pain radiating into the back(attacks may be
features
Clinical

precipitated by alcohol abuse, overeating or the use of

opiates).
3- Malabsorption (indicates >90% exocrine function
destroyed.
4- Type 1 diabetes mellitus ( 70% of cases).
 Chronic pancreatitis

● Requires a high degree of suspicion.

● Gallstone-induced obstruction may be evident as
jaundice or elevation in serum levels of alkaline
phosphatase.
● Serum amylase is variable and less reliable than in
acute disease.
Diagnosis

● Lipase in chronic pancreatitis is not useful.

● Calcification within the pancreas by computed
tomography (ct scan) and ultrasonography.(the most
useful)

Plain abdominal radiography

shows coarse dystrophic
calcification in the distribution
of the pancreas.

● Not an immediately life-threatening condition.

● The long term outlook for individuals with chronic
pancreatitis is poor, with a 20 to 25 year motility rate
Prognosis

of 50%.
● Pancreatic exocrine insufficiency, chronic
malabsorption,and diabetes mellitus can all lead to
significant morbidity and contribute to mortality.
● In other patients severe chronic pain is a dominant
problem.
● Pancreatic pseudocysts in about 10% of patients.
● Patients with hereditary pancreatitis, have a 40%
lifetime time risk of developing pancreatic cancer.
(Whether this increased cancer risk extends to other forms
of chronic pancreatitis is unclear)

1- Abstain from alcohol.

Treat-
ment

2- Simple analgesics or NSAIDs.

3- Fat soluble Vitamins.
 Chronic pancreatitis

Pathogenesis:
● Most often follows repeated episodes of acute pancreatitis
● Chronic alcohol ingestion results in the secretion of protein-rich
pancreatic fluid, which leads to the deposition of inspissated protein
plugs and obstruction of small pancreatic ducts

Chronic pancreatic local production of

promote fibrosis
injury (whatever its leads to inflammatory
and acinar cell loss
cause) mediators
EXAMPLE

- transforming growth factor β (TGF-β

- platelet-derived growth factor (PDGF

● TGF-β and PDGF result in

proliferation of secretion of remodeling of the
myofibroblasts collagen extracellular matrix (ECM)

acute: Distraction of the acinar epithelium=>secondary inflammation

=>affection of blood vessels =>hemorrhage and edema but the parenchyma
itself does not affected => the affected acinar can be regenerated and back to
normal
chronic: ethanol/oxidative stress/injury to the epithelium=>inflammation
=> release TGF beta and PDGF => proliferation of stellate cells around the
acinar cell=> collagen secretion and ECM remodulation=>calcification and
fibrosis =>pancreatic insufficiency

the difference between acute and chronic pancreatitis

Acute pancreatitis Chronic pancreatitis

Acinar injury results in release of Repeated episodes of acinar cell injury lead
proteolytic enzymes, leading to to the production of TGF-β and PDGF,
activation of the clotting cascade, acute resulting in proliferation of myofibroblasts,
inflammation, vascular injury, and edema. secretion of collagen and irreversible loss of
In most patients, acinar cell mass, fibrosis, and pancreatic
complete resolution of the acute injury insufficiency
occurs with restoration of
acinar cell mass.
 Summary

Acute Pancreatitis Chronic pancreatitis

is characterized by irreversible
— is a form of reversible injury of the pancreas leading to
pancreatic parenchymal injury fibrosis, loss of pancreatic
associated with inflammation. — parenchyma, loss of exocrine and
endocrine function, and high risk of
Acute pancreatitis may be caused by developing pseudocysts —
1. Excessive alcohol intake
2. Pancreatic duct obstruction (e.g., Chronic pancreatitis may be idiopathic
gallstones) or caused by:
3. Genetic factors (e.g.,PRSS1,SPINK1) 1. Repeated bouts of acute pancreatitis
4. Traumatic injuries 2. Chronic alcohol abuse
5. Medications 3. Germline mutations in genes such as
6. Infections (e.g., mumps) CFTR
7. Metabolic disorders leading to 4. Malnutrition (most common cause in
hypercalcemia developing countries)
8. Ischemia 5. Autoimmune disorder
— The key feature of all of these causes 6. Long-standing obstruction of the
is that they promote the inappropriate pancreatic duct by calculi or neoplasms —
activation of digestive enzymes within
the substance of the pancreas — Clinical feature include:
intermittent or persistent abdominal
Clinical features include: pain, intestinal malabsorption and
acute abdominal pain, systemic diabetes
inflammatory response syndrome, and
elevated serum lipase and amylase
levels
 Pathoma
Acute and chronic pancreatitis

EXOCRINE PANCREAS
I. ANNULAR PANCREAS
A. Developmental malformation in which the pancreas forms a ring around the
duodenum; risk of duodenal obstruction

II. ACUTE PANCREATITIS

A. Inflammation and hemorrhage of the pancreas
B. Due to autodigestion of pancreatic parenchyma by pancreatic enzymes
1. Premature activation of trypsin leads to activation of other pancreatic enzymes.
C. Results in liquefactive hemorrhagic necrosis of the pancreas and fat necrosis of the
peripancreatic
D. Most commonly due to alcohol and gallstones; other causes include trauma,
hypercalcemia, hyperlipidemia, drugs, scorpion stings, mumps, and rupture of a
posterior duodenal ulcer.
E. Clinical features
1. Epigastric abdominal pain that radiates to the back
2. nausea and vomiting
3. Periumbilical and flank hemorrhage (necrosis spreads into the periumbilical soft tissue
and retroperitoneum)
4. Elevated serum lipase and amylase; lipase is more specific for pancreatic damage.
5. Hypocalcemia (calcium is consumed during saponification in fat necrosis)
F. Complications
l. Shock- due to peripancreatic hemorrhage and fluid sequestration
2. Pancreatic pseudocyst-formed by fibrous tissue surrounding liquefactive necrosis and
pancreatic enzymes
i. Presents as an abdominal mass with persistently elevated serum amylase
ii. Rupture is associated with release of enzymes into the abdominal cavity and
hemorrhage.
3. Pancreatic abscess-often due to E coli; presents with abdominal pain, high fever, and
persistently elevated amylase
4. DIC and ARDS

III. CHRONIC PANCREATITIS

A. Fibrosis of pancreatic parenchyma, most often secondary to recurrent acute
pancreatitis
1. Most commonly due to alcohol (adults) and cystic fibrosis (children); however, many
cases are idiopathic.
B. Clinical features:
I. Epigastric abdominal pain that radiates to the back
2. Pancreatic insufficiency-results in malabsorption with steatorrhea and fat soluble
vitamin deficiencies. Amylase and lipase are not useful serologic markers of chronic
pancreatitis.
3. Dystrophic calcification of pancreatic parenchyma on imaging; contrast studies reveal
a 'chain of lakes' pattern due to dilatation of pancreatic ducts.
4. Secondary diabetes mellitus-late complication due to destruction of islets
5. Increased risk for pancreatic carcinoma
Questions
1. Chronic pancreatitis is 5. In pancreatitis, inflammation is
characterized by long-standing caused when:
inflammation of the pancreas with A. Pancreatic enzymes escape into the
......: pancreatic tissue and begin to digest
A. At later stages inflammation of the the pancreas itself
endocrine parenchyma B. Gallstones obstruct the cystic duct
B. Fibrosis C. Massive amounts of fluid
C. Inflammation of the exocrine accumulate in the peritoneal cavity
parenchyma D. Regenerative nodules are formed
D. Destruction of the ducts
6- What are the most frequent
2. The most helpful finding to laboratory findings in patients with
diagnose chronic pancreatitis is: acute pancreatitis?
A. Elevations of serum amylase A. Elevation of serum lipase followed
B. Calcifications within the pancreas by elevation of amylase.
C. Elevated levels of serum alkaline B. Normal amylase level with elevation
phosphatase. of lipase level only.
D. Persistent or recurrent abdominal C. Normal lipase level with elevation of
and back pain amylase level only.
D. Elevation of amylase levels followed
3. Which of the following by a rising of lipase.
medications commonly precipitate
chronic pancreatitis? 7. Which of the following is NOT a
A. Thiazide diuretics complication of chronic
B. Azathioprine pancreatitis?
C. Estrogens A. Pancreatic exocrine insufficiency
D. Opiates B. Malabsorption
C. Acute ischemia
4. The pancreatic ducts become D. Diabetes mellitus
extremely dilated in case of :
A. Pseudocysts of Pancreas 8. The most common etiologies of
B. Chronic Pancreatitis acute pancreatitis (AP) are
C. Acute Pancreatitis A. Idiopathic and medications.
D. Autoimmune pancreatitis B. Endoscopic retrograde
cholangiopancreatography and
gallstone
C. Abdominal trauma and pregnancy.
D. Ethanol and gallstones
 Questions
9. The most likely medication to 11. Gene mutation associated with
cause AP in a patient taking the acute pancreatitis?
following medications is: A. PRSS1, SPINK1
A. Potassium chloride B. SFTR
B. Calcium carbonate C. HLA- DR
C. Hydrochlorothiazide D. p53
D. L-thyroxine.
12. A 52 year old male present to the
10. A 30-year-old male got into a accident and emergency
road accident resulting in complaining of a severe abdominal
abdominal trauma, after pain radiating to the back. The
examination you notice a 17 cm in patient is known alcoholic . He is
diameter isolated collection of found to have increased serum
necrotic- haemorrhagic material in amylase. What is the most likely
the pancreas. What do you expect? diagnosis in this case?
A. Pseudocysts of Pancreas A. Chronic pancreatitis.
B. Chronic Pancreatitis B. Acute pancreatitis.
C. Acute Pancreatitis C. Perforated colon.
D. Autoimmune pancreatitis D. Acute appendicitis.

Answers:
1- B 2-B 3- D 4-B 5-A 6-D
7-C 8-D 9-C 10-A 11-A. 12-B

Short questions to test yourself:

1. How is chronic pancreatitis different from acute pancreatitis?
Chronic pancreatitis is defined by irreversible destruction of exocrine
pancreatic parenchyma while acute pancreatitis is a reversible condition.
2. The two most common causes of acute pancreatitis are?
-Biliary tract disease
-Alcoholism.
3.Mention some differential diagnosis of acute pancreatitis?
-Ruptured acute appendicitis.
-Perforated peptic ulcer
-Acute cholecystitis.
 ‫ﻛﻞ اﻟﺸﻜﺮ واﻟﺘﻘﺪﯾﺮ ﻟﻠﺠﮭﻮد اﻟﻌﻈﯿﻤﺔ‬
‫ﻣﻦ ﻗﺒﻞ أﻋﻀﺎء ﻓﺮﯾﻖ ﻋﻠﻢ اﻷﻣﺮاض اﻟﻜﺮام‬

‫ﻗﺎدة ﻓرﯾق ﻋﻠم اﻷﻣراض‬

‫ﺷﯾرﯾن اﻟﻌﻛﯾﻠﻲ‬ ‫ﻓﺎﯾز ﻏﯾﺎث اﻟدرﺳوﻧﻲ‬

‫اﻋﺿﺎء ﻓرﯾق ﻋﻠم اﻷﻣراض‬

‫رزان اﻟزھراﻧﻲ‬ ‫ﻣﮭﺎ اﻟﻌَ ﻣري‬ ‫راﻛﺎن ﻣﺣﻣد اﻟﻐﻧﯾم‬

‫ﻟﯾن اﻟﺣﻛﯾم‬ ‫ﻣﺟد اﻟﺑراك‬ ‫ﺳﻠطﺎن ﻧﺎﺻر اﻟﻧﺎﺻر‬
‫ﻋﮭد اﻟﻘرﯾن‬ ‫ﺑﺗول اﻟرﺣﯾﻣﻲ‬ ‫ﻋﺎدل ﻋﺑداﻟﻌزﯾز اﻟﺳﺣﯾﺑﺎﻧﻲ‬
‫وﺟدان اﻟﺷﺎﻣري‬ ‫ﻣﻧﯾرة اﻟﻣﺳﻌد‬ ‫ﺣﺳن ﻣﺣﻣد اﻟﻌرﯾﻧﻲ‬
‫ﻏرام ﺟﻠﯾدان‬ ‫ﻣﺷﺎﻋل اﻟﻘﺣطﺎﻧﻲ‬ ‫ﺗرﻛﻲ ﻋﯾد اﻟﺷﻣري‬
‫ﻟﯾﻠﻰ اﻟﺻﺑﺎغ‬ ‫رِ ﻧﺎد اﻟﻔرم‬ ‫ﺳﻠطﺎن ﺑن ﻋﺑﯾد‬
‫رِ ﯾﻧﺎد اﻟﻐرﯾﺑﻲ‬ ‫ﻏﺎدة اﻟﺣﯾدري‬ ‫ﻋﺑداﻟﺟﺑﺎر اﻟﯾﻣﺎﻧﻲ‬
‫ﻧورة اﻟﻘﺎﺿﻲ‬ ‫داﻧﺔ اﻟﻘﺎﺿﻲ‬ ‫ﻋﺑدﷲ اﻟﻣﻌﯾذر‬
‫ﻣﮭﺎ ﺑرﻛﮫ‬ ‫ﻣﻧﺻور اﻟﻌﺑرة‬
‫ﺗرﻛﻲ آل ﯾﻧﮭﺎر‬
‫ﺳﻌد اﻟﻔوزان‬
 ،‫ﻟﻠﻔﺷل‬ ‫ﻗد ﺗﺗﻌرض‬
‫ﻟﯾس ﻻﻧك ﻻ ﺗﺳﺗطﯾﻊ ﻟﻛن ﻟﺗﺗﻌﻠم‬
‫ ﻟﺗﻧﮭض‬،ً ‫درﺳﺎ ً ﻟِﺗُﺻﺣﺢ ﺧطﺄ‬
‫ﻣﺟدداً ﻓﺄﻧت ﺗﺳﺗطﯾﻊ‬

Best of luck.

References:
*Slides/Pathoma/Robbins

Any questions/comments and

suggestions:
* EMAIL: [email protected]
*TWITTER : @pathology437