Anatomy

• The pancreas lies in the epigastrium and left hypochondrium, crossing the midline at the level of L1 to
L3.
• Retroperitoneum organ, posterior to the stomach and anterior to the IVC, superior mesenteric, portal
and splenic veins, vertebral column, the aorta, and splenic artery and the left kidney.
• It is comprised of:
◦ Head: lying in the C-loop of the duodenum.
◦ Neck: is that part of the pancreas overlying the superior mesenteric and portal veins as they
course towards the liver.
◦ Body
◦ Tail: lying within the hilum of the spleen.
◦ Uncinate process: a projection arising from the lower part of the head and extending medially to lie
beneath the body of the pancreas. It lies posterior to the superior mesenteric vessels.
Sometimes the pancreas fails to develop normally and there may be congenital defects associated with
the uncinate process. The uncinate process may split and encircle the duodenum, which is known as an
annular pancreas.

The common bile duct lies in a groove on the posterior superior surface of pancreatic head.
Typically, the pancreas is drained by 2 ducts, the main and accessory ducts. The main duct runs through
the entire gland receiving tributaries from it and exits into the duodenum via the ampulla of Vater where it
is in close relationship with the common bile duct. The accessory duct drains the head and has a separate
opening into the duodenum.
Physiology
Digestive enzymes are secreted by acinar cells into the pancreatic ducts which then drain into the
intestinal lumen to facilitate digestion and absorption. Pancreatic juice is alkaline and has a high HCO3‾
content; this together with bile and intestinal juice which are also neutral or alkaline neutralize gastric acid.
Approximately 1500 ml of pancreatic juice is produced per day, under the influence of secretin and
cholecystokinin.
Pancreatic juice contains trypsinogen which is converted to trypsin by the brush border enzyme
enterokinase when pancreatic juice enters the duodenum. Trypsin converts pro-enzymes (zymogens) in
pancreatic juice into active enzymes as well as further trypsinogen into trypsin in an autocatalytic chain
reaction. Thus, the release into the pancreas of even a small amount of trypsin results in a chain reaction
that produces active enzymes that can digest the pancreas.
Trypsin also activates phospholipase A2 which forms lysolecithin from lecithin, a normal constituent of
bile. Lysolecithin damages cell membranes causing disruption of pancreatic tissue and necrosis of
surrounding fat.

Various hormones are produced and secreted by the islets of Langerhans in the pancreas, including
insulin, glucagon, somatostatin, pancreatic polypeptide and others.

Pathophysiology
The pathogenesis of AP is caused by an premature activation of trypsinogen to trypsin in the pancreatic
cells (normally this only occurs when trypsinogen is secreted into the duodenum). Once activated, these
enzymes are responsible for auto-digestion of pancreatic tissues which result in necrosis and in severe
cases stimulate the production of inflammatory cytokines and neutrophils which in turn triggers an
inflammatory cascade causing a systemic inflammatory response syndrome (SIRS). SIRS may develop
into an acute respiratory stress syndrome (ARDS), multi-organ dysfunction syndrome (MODS) or organ
failure. The mechanism by which trypsin is activated in the pancreatic acini remains uncertain (just
theories).

The mechanisms in alcohol induced and other causes of pancreatitis are even less clear but, in principle,
intracellular protective mechanisms to prevent trypsinogen activation or reduce trypsin activity are
overwhelmed. Genetic predisposition, such as mutation of the cationic trypsinogen gene may promote AP
in the presence of alcohol.
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4. ACUTE PANCREATITIS
Acute Pancreatitis Medical Editor: Maxine, Jude and Sarah

OUTLINE Acute pancreatitis refers to an acute inflammation of the

pancreas, accompanied by abdominal pain and elevation of
I) QUICK REVIEW OF THE PANCREAS serum pancreatic enzymes [Hopkins medicine]
II) MECHANISM OF ACTION
III) ETIOLOGIES
SUMMARY OF ETIOLOGY OF ACUTE PANCREATITIS
IV) PATHOPHYSIOLOGY
V) DIAGNOSIS
VI) TREATMENT
VII) APPENDIX
VIII) REFERENCES
I) QUICK REVIEW OF THE PANCREAS
Pancreas is both an endocrine and exocrine organ but, in this lecture, we will focus more on the exocrine (secretory) portion of
the pancreas, which secretes many digestive enzymes.

DUCTAL SYSTEM OF THE PANCREAS FORMATION OF THE GRANULES:

The small pancreatic ducts join together to form the main
pancreatic duct, which connects to the duodenum.

The pancreas secretes pancreatic enzymes and

bicarbonate rich fluid into the duodenum.

These pancreatic juices interact with enteropeptidase in

the duodenum leading to activation of these zymogens. Function of the Granules:
Contain zymogens which are the inactive form of the
enzyme

RECALL:
There are different types of zymogens:
 Lipases
 Amylase
 Proteases

The zymogens need to remain inactivate until they reach

the duodenum where they can break down the nutrients of
Figure 1. Pathway of pancreatic enzyme secretions our diet. This is achieved by the protease inhibitors.

Components of the pancreatic ducts:

Ductal epithelium Figure 2. Content of Granules in Acinar Cells. The protease
o These are the cells lining the ducts inhibitors allows the zymogens to remain inactive while in the
pancreas
 Makes bicarbonate rich pancreatic fluid

Acinar cells
o Found in the end of the ducts
 Secretory cells that make digestive enzymes

Granules (Vesicles):
o Found in the acinar cells

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II) MECHANISM OF ACTION III) ETIOLOGIES

(A) GALL STONES (MOST COMMON CAUSE)

Damage to the pancreas that alters the secretion of
enzymes into the duodenum via 2 ways: RECALL:
In the gall bladder the cystic duct fuses with the common
(A) OBSTRUCTION WITHIN THE DUCTS hepatic duct to form the common bile duct.
Any cause of accumulation of the enzymes: o Common bile duct fuses with the main pancreatic duct
o ↑ Pressure between the ducts to form the hepatopancreatic ampulla (or Ampulla
o Alters the normal movement of enzymes and of Vater).
excretion of the zymogens

This pressure buildup causes the lysosomes inside the

acinar cells to fuse with the granules containing the
zymogens.

Lysosomes then activate the zymogens leading to

secretion of the activated proteases in the pancreas.
This leads to AUTO DIGESTION OF THE PANCREAS
o Hence acute pancreatitis

(B) DIRECT DAMAGE OF THE ACINAR CELLS

Any damage to the acinar cells stimulates the same
process of lysosomal fusion with the granules
Leading to activation of zymogens and auto digestion
of the pancreas
Figure 4. Ductal System in Pancreas and Gall Bladder [Wikipedia]
Remember these 2 processes as they will be referred to
over and over again throughout the lecture. Pathophysiology:
Gall stone obstructs the hepatopancreatic ampulla

(B) ETHANOL
Usually occurs in those with chronic pancreatitis due to
alcohol abuse, which develop an acute exacerbation of the
chronic pancreatitis.
Figure 3. Mechanism of Action on Ductal Epithelium and Acinar
Cells of the Pancreas Ethanol can cause acute pancreatitis in 3 ways:
(1) Through direct stimulation of acinar cells
This increases the release of zymogens.
As they accumulate in the ducts, some zymogens are
Table 1. Summary of MoA of Acute Pancreatitis undesirably activate.
Mechanism of Action (2) Stimulation of the ductal epithelial cells
Obstruction Destruction
Ethanol can stimulate the ductal epithelial cells to secrete
↑ Pressure between the Damage to the acinar cells thick bicarbonate rich secretion.
ducts stimulates the fusion of
o This obstructs the ducts and repeats the same
Alters the normal lysosomes with the
process of autodigestion of the pancreas.
movement of enzymes granules
and excretion of the (3) Activation of neutrophils
zymogens Ethanol stimulates neutrophils
Neutrophil increases production of ROS and proteases
The lysosomes inside the acinar cells to fuse with the
which lead to direct destruction of acinar cells
granules containing the zymogens.
o Zymogens are released and proteases are activated
Lysosomes then activate the zymogens leading to
leading to autodigestion of the pancreas.
secretion of the activated proteases in the pancreas.

This leads to AUTO DIGESTION OF THE PANCREAS

leading to acute pancreatitis

Figure 5. The 3 ways in which ethanol can cause acute pancreatitis

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(C) PENETRATING TRAUMA (F) MUMPS VIRUS

Any penetrating trauma caused by sharp objects that The Mumps virus can cause acute pancreatitis in 2 ways:
affects the pancreas can cause acute pancreatitis.
Pathophysiology:
Pathophysiology: 1. Directly act on the ductal epithelial cells and
Penetrating trauma can cause direct injury to the acinar destroy them
cells in the pancreas. 2. Directly acts on the acinar cells, causing the
o This repeats the same process of zymogen release release of zymogens
and activation of proteases These 2 causes lead to the same process previously
 leading to autodigestion of the pancreas described in the mechanism of action of acute pancreatitis.

(D) HYPERTRIGLYCERIDEMIA

RECALL:
Triglycerides are absorbed in the GI tract and packaged
in enterocytes into lipoproteins called chylomicrons
In case of a genetic disorder or high absorption of
triglycerides, there will be high levels of chylomicrons Figure 7. Steroids and Mumps cause of Acute Pancreatitis
in the blood circulation.
Pathophysiology: (G) AUTOIMMUNITY
If there are increased amount of chylomicrons in the blood, In most autoimmune diseases there is damage to many
they can obstruct the capillaries that supply the pancreas. organs including the pancreas. For example IgG4
antibodies produced in conditions like SLE, RA.
This leads to: Pathophysiology:
o ↓↓ in oxygen supply
Autoantibodies can directly destroy the ductal epithelial
 Ischemic tissue develops → necrosis of pancreatic
cells and acinar cells and repeat the same process of
tissue → pancreatitis
autodigestion of the pancreas.

(H) SCORPION BITES

In scorpion bites, toxins are released that can cause
Figure 6. Hypertriglyceridemia causing necrosis of the destruction of ductal epithelial cells and acinar cells.
pancreas

(E) STEROIDS
Corticosteroids can stimulate the ductal epithelial cells to
create thick secretions

Pathophysiology: (I) DRUGS

o Thick secretions in the ductal epithelium can build up Some drugs can cause adverse effects leading to acute
and cause obstruction of the pancreatic ducts. pancreatitis. These include:
 This leads to pressure build up and altering the Sulfa drugs
normal movements of zymogens. HIV medication (especially NRTIs & protease inhibitors)
• Zymogens are activated in the pancreas DM medications (GLP-1)
instead of the digestive system leading to
destruction of pancreas.

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(J) ENDOSCOPIC RETROGRADE (K) HYPERCALCEMIA:

CHOLANGIOPANCREATOGRAPHY (ERCP) High concentration of calcium in the blood can be
distributed to certain tissues like the pancreas.
This procedure is performed for:
o Gall stone diagnosis (e.g. to identify the cause of Pathophysiology:
acute pancreatitis) Calcium can directly stimulate the zymogens, and
o Removal of gall stones protease activation.
This leads to auto digestion of the pancreas.

Pathophysiology:
The endoscope reaches the hepatopancreatic ampulla
o An incision is made in the sphincter to reach the
common bile duct where gall stones can be found.

HOWEVER, this can lead to damage to pancreatic tissue

and destruction of the acinar cells
o This causes the release of zymogens and the process
repeats again.
Figure 9. Hypercalcemia causing activation of zymogens in
granules

TO REMEMBER THE ETIOLOGIES:

I GET SMASHED

alcohol induced pancreatitis, a history of heavy alcohol intake of 5-10 years is

usually obtained. The attack comes on typically the "afternoon after the night
Figure 8. ERCP procedure showing device entering the
before". Gallstones or carcinoma of the pancreas should be considered in the
hepatopancreatic ampulla to remove the gall stones. middle aged or elderly patient, particularly when there is little or no alcohol history.
[GICenterTexas]. This procedure can cause potential damage With gallstones, the attack typically comes on after a large meal which stimulates
to the acinar cells gallbladder contraction (by the release of cholecystokinin).

4 of 17 GASTROINTESTINAL PATHOLOGY: Note #4. Acute Pancreatitis

 SUMMARY OF ETIOLOGY OF ACUTE PANCREATITIS

Table 2. Summary of Etiologies with the help of a mnemonic

Obstruction or
Mnemonic Etiology Description
Destruction?
Idiopathic -
I

Unknown

Gall Stones Gall stone obstructs the hepatopancreatic ampulla Pancreatic

Obstruction
Enzymes cannot be secreted, so they accumulate.
Ethanol 1- Stimulation of Acinar Cells
GET

2-Stimulation of Ductal Epithelial Cells Both

3-Activation of neutrophils

Trauma
Penetrating trauma causes injury to acinar cells Destruction

Steroids
Stimulate ductal epithelial cells to produce thick secretions Obstruction

Mumps 1-Damage of Acinar Cells

Destruction
2-Damage of Ductal Epithelial Cells

Autoimmunity Autoantibodies can directly destroy the ductal epithelial cells

Destruction
and acinar cells

Scorpion bite Toxins released tcan cause destruction of ductal epithelial

Destruction
S M AS HE D

cells and acinar cells.

Hypertryglceridemia Chylomicrons in the blood can obstruct the capillaries that
supply the pancreas.
Both
This leads to: ↓↓ in oxygen supply
Ischemic tissue develops → necrosis of pancreatic tissue
→ pancreatitis
Hypercalcemia AfraTafreeh.com
Calcium can directly stimulate the zymogens, and protease
activation. Destruction
This leads to auto digestion of the pancreas.
ERCP An incision is made in the sphincter to reach the
Destruction
common bile duct but this can lead to damage to pancreatic
tissue and destruction of the acinar cells

Drugs Sulfa drugs

HIV medication (especially NRTIs & protease inhibitors) Destruction
DM medications (GLP-1)

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 *SA book; The diagnosis of pancreatitis requires 2 of the following:
1. Abdominal pain consistent with acute pancreatitis (acute onset,
epigastric, severe, often radiating to the back).
2. Serum lipase or amylase ≥3x normal
IV) PATHOPHYSIOLOGY 3. Characteristic ndings on CT or MRI scan

(A) CLINICAL FEATURES

(1) Epigastric Abdominal Pain (2) Gastrointestinal Disturbances

Figure 10. Characteristics of epigastric pain.

(i) Abdominal Distension, Nausea and Vomiting
↑Inflammation → pain
o Pancreas is located within the epigastric quadrant Inflammation of pancreas causes inflammation or
compression of the nearby structures (duodenum and the
(i) Characteristics: stomach)
Constant epigastric pain
o As compared to intermittent pain of peptic ulcer,
which is dependent on the timing of meals
o May lead to abdominal distension due to the
o In some cases, the pain may be in the right upper
obstruction of the pancreas to the gastric and
quadrant (RUQ) or left upper quadrant (LUQ) [Vege, 2021]
duodenal lumen
Radiates to the back o Severe abdominal distension
Laying supine makes the pain much worse
o Due to ↑stretch → pain
Leaning forward makes the pain better
(ii) Ileus
Table 3. Characteristics (OPQRST) of epigastric pain in acute Inflammation can also affect the motility of nearby
pancreatitis. structures (i.e. small intestine) → ileus
Onset Acute onset o Ileus: ↓contraction of the smooth muscle
Palliative or
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Palliative: leaning forward o Can present as a physiologic bowel obstruction →
Provoking: supine position less bowel sounds in physical exam
provoking factors
Quality *Varies (3) Jaundice
Radiation Radiates to the back If gallstone is present in hepatopancreatic ampulla
Severity Severe
Time *Varies

Gallstones are the most common cause of acute

pancreatitis (40-70%) [Vege, 2021]
o Risk of developing acute pancreatitis with gallstones
The onset of acute pancreatitis is de ned as the time of is greater in men but incidence is greater in women
onset of abdominal pain. Once the diagnosis of due to higher prevalence of gallstones
pancreatitis has been made and an estimation made as to
the time of onset, it is important to grade the severity of
the attack in order to identify those who require transfer
to specialist care and aggressive early treatment. Three
degrees of severity are de ned, again by the 2012 revised
Atlanta classi cation:
1. Mild acute pancreatitis (80% of patients)
a. No organ failure
b. No local or systemic complications

2. Moderately severe acute pancreatitis

a. Transient organ failure that resolves within 48 hours
b. Local / systemic complications without persistent organ
failure

3. Severe acute pancreatitis

a. Persistent single / multiple organ failure
lasting >48 hours

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 (B) COMPLICATIONS

(2) Complications in Coagulation

Figure 12. Coagulation complications of acute pancreatitis.

IL-1, IL-6, and TNF-α have different effects on different
organs
Act on the coagulation enzymes = ↑procoagulant and
↓anti-coagulant protein activity
As a result:
o Increased clots
o Consumed clotting proteins → ↑bleeding
 The next time the body needs these proteins, they
are insufficient to form clots and blood leaks out
Figure 11. Complications of acute pancreatitis. of the vessels

Significant inflammation of the pancreas Disseminated Intravascular Coagulation

o Condition characterized by widespread blood clots
and bleeding
(3) Complications in Hypothalamus, Bone Marrow and
Liver
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o Chemokines and inflammatory mediators try to attract
or pull in WBC in the inflamed area
(1) Complications in the Cardiovascular System
Neutrophils can also stimulate macrophage to release IL-
1, IL-6 and TNF-α that act on blood vessels to undergo a
vasodilatory response and increase permeability (leaky)
→ fluids can leak into the interstitial space
As a result:
o Vasodilation
Figure 13. Effects of IL-1, IL-6 and TNF-α on the hypothalamus,
red bone marrow and the liver.
o ↑capillary permeability
(i) Hypothalamus
 Less fluid WITHIN the vessel = ↓EAV IL-1, IL-6, and TNF-α can also stimulate the
Vasodilation is widespread hypothalamus = ↑temperature = fever
o “This inflammation is infection-related. If we increase
the temperature, bacteria can’t survive in any way”

(ii) Red Bone Marrow

These cytokines can also stimulate the bone marrow to
produce neutrophils and other leukocytes (WBCs)
o ↑HR is supposed to ↑cardiac output and eventually → leukocytosis
↑BP
(iii) Liver
↓EAV
Cytokines stimulate the liver to synthesize and release
acute-phase reactant proteins (ARP)
o To alert other organs of the inflammation
o Types:
 CRP (C-reactive protein)
 ESR (erythrocyte sedimentation rate)
o Measures of inflammation
 Therefore, in acute pancreatitis, ↑CRP and ↑ESR

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(4) Pulmonary Edema (6) Ascites
Recall the widespread vasodilatory and increased ↑capillary permeability in the abdomen (within the
permeability secondary to the release of cytokines retroperitoneal cavity)
↑capillary permeability in the lungs

o Can occur diffusely throughout multiple alveoli

Worst-case scenario: ARDS (acute respiratory distress
syndrome)
o #1 cause of mortality in patients with acute
pancreatitis

(7) Acute Kidney Injury

Vasodilation and ↑capillary permeability

Pre-renal AKI
o Due to ↓blood volume
o ↑↑BUN and ↑Cr due to low blood volume in the
kidneys because of third-spacing or ↓perfusion

(5) Pleural Effusion

Pancreas can fistulize through the diaphragm

Rare

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 Local complications
(C) SEVERE COMPLICATIONS
Proteases and lipases released can damage the pancreas through autodigestion

(1) Liquefactive Necrosis, Pseudocyst and Pancreatic Abscess (2) Hemorrhagic Necrosis

Figure 14. Complications secondary to liquefactive necrosis.

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Lipases break down the peripancreatic fat tissue →
liquefactive necrosis Figure 15. Complications secondary to hemorrhagic necrosis.
Liquefactive necrosis
o Some of the pancreatic tissues release triglycerides (i) Hypovolemic Shock
as a response
Autodigestion by proteases and lipases
o Triglycerides then get broken down to free fatty acids
If the proteases and lipases extend beyond the pancreas,
(FFA)
they can destroy the pancreatic tissues and the blood
o FFA loves to combine with Ca2+ → ↓Ca2+ in the blood
vessels nearby → hemorrhagic necrosis
(hypocalcemia)
o Worst case scenario: it erodes to a near aortic vessel
 Saponification: formation of metallic salt of a fatty
→ hypovolemic shock and bleeding
acid
o Hypovolemic shock because of massive rupture
(i) Pseudocyst (ii) Retroperitoneal Bleeding
Fluid collections due to liquefactive necrosis → fibrous
Because of bleeding, blood can accumulate in the
tissue surrounds a fluid collection = pseudocyst
retroperitoneum
o Pseudocyst: fluid collection walled-off with fibrous
o Recall that the pancreas is located in the retroperitoneum
tissue
o Can be asymptomatic but can compress different Signs of Retroperitoneal Bleeding:
structures if large enough o Cullen’s Sign
 Can compress near the bile duct → jaundice  Bleeding/bruising in the subcutaneous fatty tissue
 Can compress the duodenum → obstructive Sx around the umbilicus
 “C-shaped” bleed or bruise in the umbilicus
(ii) Pancreatic Abscess o Grey-Turner Sign
In some situations, pancreatic pseudocyst can be  Bruising of the flanks
infiltrated with E. coli → causes bacterial infection →
Ecchymosis in the
pancreatic abscess anks (Grey Turner’s
o Symptoms: very painful, fever, severe abdominal sign) or in the peri-
pain, intense leukocytosis, stays around umbilical region
(Cullen’s sign) occur in
o Can happen around ≥4 weeks
about 3% of patients
and are considered
(iii) Infected and Sterile Liquefactive Necrosis signs of severe disease.
Infected liquefactive necrosis
o Fluid collection secondary to liquefactive necrosis is
infiltrated by pathogens (usually bacteria)
Sterile liquefactive necrosis Figure 16. Cullen's (A) and Grey-Turner sign (B) indicative of
o Fluid collection is not infected or is sterile retroperitoneal hemorrhage [Wright, 2016].

Acute Pancreatitis GASTROINTESTINAL PATHOLOGY: Note #4. 9 of 17

 V) DIAGNOSIS
(A) CLINICAL
(1) Classic Signs and Symptoms (2) Risk Factors
Epigastric abdominal pain History of gallstones
Constant radiating to the back Alcoholic
Aggravating factor: lying supine Hypertriglyceridemia
Alleviating factor: laying forward
Associated: nausea, vomiting

(B) LABORATORY WORK-UP

Table 4. Laboratory work-up for patients suspected of having pancreatitis.
Test Rationale

Higher specificity
3x upper limit of normal – indicative of pancreatitis
Serum O RECALL:
Lipase Destruction of pancreas  releases
(High lipases
yield) Lipases causes liquefactive necrosis
 saponification reaction  released
into nearby vasculature

Serum Not as good, lower specificity since it is released from multiple different areas
Amylase (i.e. Salivary glands released when intubating a patient with pancreatitis)
3x upper limit of normal – indicative of pancreatitis

Hematocrit:
o 45% RBC, <1% buffy coat, 55% plasma
o Formula: RBC / total blood (buffy coat + plasma layer)
o Pancreatitis:
 ↑ 3rd spacing  ↑ Leaky vessels  ↑ Plasma leaks out = ↓ plasma
 If ↑ RBC / ↓ total blood = then ↑ Hematocrit = Hemoconcentration
CBC
↓ Hemoglobin:
o Pancreatic inflammation  necrosis or destruction of nearby vessels 
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o ↑ blood leakage into retroperitoneum
↑ WBC:
o ↑ Neutrophils / leukocytosis

Lipid Triglyceride level:

panel o ≥1000 mg/dL – significant level to cause pancreatitis

Hypercalcemia: might be the cause of pancreatitis

Calcium Hypocalcemia: Complication due to liquefactive necrosis or saponification 
free fatty acids released and complex with calcium

↑ BUN, Creatinine
BNP o ↓ Effective arterial blood volume  ↓ perfusion to kidneys 
o ↓ Urine output  ↓ GFR  ↓ urea excretion

Acute
phase ↑ ARP: ↑ CRP (intermediate specificity)
reactants o When macrophages release IL-1 & IL-6  act on the liver

Pro- If suspecting infection

calcitonin Pancreatitis with infection (infected necrosis) OR presence of abscess
Clinical manifestation: Fever, hypotension, tachycardia, leukocytosis

Hyperbilirubinemia (↑ Bilirubin):
Liver o Gallstone lodged in hepatopancreatic ampulla
Function  Retrograde flow (backs up) into liver  gallbladder
Test Liver injury  ↑ AST, ↑ ALT
o Bile accumulates against blockage  ↑ pressure from lodged stone

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(C) IMAGING
To look at the grading and severity
Look for any complications
(1) Right Upper Quadrant ultrasound

Figure 17. RUQ Ultrasound. CBD dilation due to downstream gallstone.

Advantage:
o May tell you the exact cause quickly
 Evidence of gallstone
 Ductal dilation
o Pick up fluid collections
 Pseudocyst
 Walled-off necrosis

Disadvantages:
o Hard to use for ↑ enlarged abdomen (i.e. distention, ↑ bowel
gas)
 May obstruct the view of pancreas

Ultrasound Impression:
o Gallbladder’s neck is connected to the cystic duct that fuses
with the common hepatic duct (CBD) to form the bile duct
o If CBD ≥10 mL  significant dilation
 Suspect that there’s something downstream that is
plugging the biliary duct  gallstone pancreatitis

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(2) Magnetic resonance cholangiopancreatography (3) Endoscopic retrograde cholangiopancreatography
(MRCP) (ERCP)

Figure 18. Gallstone pancreatitis via MRCP. Figure 19. Gallstones seen in ERCP may be removed.

Purpose: Purpose:
o MRI which looks at particularly the entire o Diagnostic and therapeutic
pancreaticobiliary system o Run the camera/ catheter down through the
o Looks at any kind of filling defect or any point where duodenum up through the pancreatic duct  biliary
there’s a stone or blockage at some part of the system + administer contrast
hepatopancreatic ampulla and biliary system  To see any kind of gallstone or issue
o If (+) stone  extract
Indication:
o Inconclusive ultrasound
Indication:
 Unknown for presence of ductal dilation / stone o High suspicion of pancreatitis
o Non-specific results related to pancreatitis o UNSTABLE patient

MRCP Impression:
o Area of biliary tract (gallbladder  cystic duct  ERCP Impression:
common hepatic duct  common bile duct): o Catheter is seen coming down endoscopically which
 Assess for any kind of filling defect through the course through structures:
biliary tract  Pancreatic ampulla
o Gallstones at the common bile duct:  Near the area of main pancreatic duct
 Dark areas that may be blocking the contrast  Up to the common bile duct
o Main pancreatic duct should fuse with common bile o Dilation at the area of:
duct:  biliary duct
 See mild ductal dilation around the head of the  hepatopancreatic ampulla
pancreas  gallstone pancreatitis o Differential diagnosis:
 Gallstone pancreatitis
 Choledocholithiasis
 Complications: Ascending cholangitis

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(4) CT Scan
Purpose:
o Shows peripancreatic fat stranding
 but in acute phase  harder to see due to
increased inflammation and hard to demarcate
margins of the pancreas
o Shows necrotic tissues surrounding the pancreas
o Shows fluid-filled cysts

Indication:
o Looking for complications of pancreatitis (i.e. after
weeks, symptoms of pancreatitis still persist)
 Pancreatic pseudocyst: fluid collection that’s
encapsulated
 Abscess: fluid collection that looks loculated +
infectious material in it
 Necrosis: infected / hemorrhagic / bleeding Figure 21. Necrotizing pancreatitis: complication which may be
found at the later stages of pancreatitis.
o Best for unclear diagnosis

CT Scan Impression: o When looking for complication, do it at the later

stages of pancreatitis:
o Structures:  ↑↑ inflamed pancreas  cannot demarcate
 Pancreas pancreas’ margins anymore
 Splenic vessels at the posterior edge of the  Fluid collections
pancreas  Necrosis around the vicinity of pancreas
 Differential diagnosis:
• Necrotizing pancreatitis

Figure 20. Pancreatic fat stranding indicative of pancreatitis in

CT Scan.

o Peripancreatic fat stranding indicative of

pancreatitis:
 Edematous
 White stranding of matter around pancreas Figure 22. Pancreatic pseudocyst.
o In line with clinical manifestation: o Massive pancreatic pseudocyst
 Abdominal pain  Compresses nearby ureter  hydronephrosis
 Nausea and vomiting  Symptoms seen 4 weeks after acute pancreatitis
 Fatigue
 ↑ Lipase 3x the upper limit of normal

Acute Pancreatitis GASTROINTESTINAL PATHOLOGY: Note #4. 13 of 17

(5) Abdominal X-Ray
Purpose:
o Show dilation of the nearby small bowel (sentinel
loop) due to ↑ inflammation of the pancreas
o Show inflammation at the tail of the pancreas near
the splenic flexure
 ↑ inflammation and fluid collections  compresses
splenic flexure
 ↑ back pressure  ↑ dilation of bowels proximal to
splenic flexure:
• Ascending colon
• Transverse colon
 Colon cutoff sign: Dilated ascending and
transverse colon + cutoff at the splenic flexure
• Sign of pancreatitis
Indication:
o Rule out signs of bowel obstruction
o Not diagnostic

Figure 24. Colon Cutoff sign indicative of acute pancreatitis.

X-Ray impression:
o Sentinel loop which can be found in Acute
Pancreatitis:
 Due to pancreatic inflammation
 Localized ileus / bowel gas pattern that almost
looks like an obstruction but is really a non-
obstructive pattern
o Colon cutoff sign
 Explanation:
AfraTafreeh.com • Inflamed tail of the pancreases causes partial
obstruction  dilation proximal to the
obstruction
 Manifests as:
• Bowel gas pattern around the splenic flexure
 transverse colon  ascending colon
Figure 23. X-Ray impression of acute pancreatitis showing • Cutoff where the splenic flexure ends
sentinel loop.

14 of 17 GASTROINTESTINAL PATHOLOGY: Note #4. Acute Pancreatitis

 VI) TREATMENT

(1) Fluid administration (2) Analgesia

Given due to vasodilatory effect of the pancreatitis
Algorithm:
Problem: o Start with Tylenol
o ↓ BP o PRN Opioids if Tylenol doesn’t work
o Edema due to third spacing (fluid accumulated in the  Fentanyl
interstitial space i.e. lungs as pulmonary edema,  Hydromorphone
extremities as peripheral edema, abdomen as o Morphine
ascites)  Questionable: may cause spasm of sphincter of
Oddi
Types: o Low dose Ketamine infusion
o Normal Saline o Caution with the pathophysiology of Opioids:
o Lactated Ringer  ↓ Contractility of bowels  Ileus (worse)
 Some literature shows it’s superior to normal
saline

Caution!
o DO NOT push too much fluid (10-12 L) within the first
couple of hours
o Effect: ↑ Third spacing of fluid
o Risk: Fluid overload

Complications of very severe pancreatitis:

o ARDS:
 Due to the increased capillary permeability
 ↑ Fluids  overload into interstitial spaces 
lungs  worsen condition or put them into ARDS
o Abdominal compartment syndrome
 Due to ↑ fluids third spacing into retroperitoneum
and abdomen

Target improvements:
o BP: MAP goes up (3) Nutrition
o ↑ Urine output AfraTafreeh.com
o ↓ BUN Start with NPO (nil per os or nothing by mouth)
o ↓ Hematocrit  less hemoconcentration
o For Bowel rest

Option: NGT (nasogastric tube) to decompress the

bowels
o If ↑ inflammation
o ↑ pain, nausea and vomiting
o (+) Gastric outlet obstruction

Pain free
o Feed early via:
 Oral
 NGT
o Pathophysiology:
 ↑ Pancreatic inflammation  ↑ gut permeability
 Natural flora (bacteria) can pass through the gut
 Feeding early changes gastric permeability and
INHIBITS bacterial translocation  ↓ risk of
infection

Acute Pancreatitis GASTROINTESTINAL PATHOLOGY: Note #4. 15 of 17

 AfraTafreeh.com
AfraTafreeh.com
(4) ERCP ± CCY (6) Fluid Collections
Cause related treatment Due to ↑ necrosis and inflammation = ↑ fluid collections

ERCP If Sterile:
o Stone dislodged within the hepatopancreatic ampulla Observe
due to cholelithiasis DO NOT GIVE ANTIBIOTICS
o Removes stone and ↓ recurrence of stone Overtime develops fibrous tissue around the area  walls
appearance off the fluid collection + necrosis = bacterial invasion
 Tool goes through the duodenum (infected necrosis)
 Cuts open sphincter of oddi o Start Carbapenems: Meropenem, Imipenem
 Sucks out the stones o Fine-needle aspiration: to distinguish sterile necrosis
vs infected necrosis  send out for culture and gram
Cholecystectomy staining
o If with high risk of recurrence AND reduce risk  (+)  Carbapenems: Meropenem, Imipenem +
recurrence of dislodged stones Debridement (cut necrotic tissue out)
o Cuts the gallbladder • endoscopically OR percutaneously
• open necrosectomy

If (+) fibroblasts come into the area

Complication ≥4 weeks after the initial event of

pancreatitis:
o Asymptomatic  Observe
o Symptomatic  ↑ pancreatic pseudocyst  persistent
pain + compresses the following  Percutaneous
drainage
 Stomach: nausea and vomiting
 Duodenum: bowel obstructive symptoms
(5) Medications to reverse hypertriglyceridemia-  Bile duct: jaundice
induced pancreatitis o E. coli infiltrates into the pancreatic pseudocyst:
 fibrous tissue walled off infective necrosis
Hypertriglyceridemia-induced pancreatitis  Clinical manifestation: pancreatic abscess +
o Due to medications persistent abdominal pain + fever + leukocytosis +
 Propofol palpable mass
o Lipoprotein lipase enzyme deficiency  Treatment:
• Fine-needle aspiration: to distinguish
Medications: pancreatic pseudocyst vs abscess  send
o Insulin infusion: stimulates Lipoprotein lipase out for culture and gram staining
 ↑ Breaks down triglycerides  Free fatty acids + o (+)  antibiotics, drainage
Glycerol • Start antibiotics:
 ↓ triglyceride concentration  taken up by muscle, o Carbapenems: Meropenem, Imipenem
cardiac cells • CT guided drainage
o Fibrates
 ↓ triglyceride production
o ± Apheresis
 If refractory to all things
 Pulls all blood out  machine sifts all the actual
fat out  sends blood back in

16 of 17 GASTROINTESTINAL PATHOLOGY: Note #4. Acute Pancreatitis

• Don't give abx if there's no infection.

Gallstone pancreatitis is best treated by initial conservative treatment as the majority of patients will
settle spontaneously with the passage of the offending calculus into the bowel. Elective cholecystectomy
1-4 weeks after the acute attack is strongly recommended to pre-empt a possible second attack. Earlier
intervention is sometimes required in the small group of patients with progressive jaundice with or without
associated cholangitis. In this situation an ERCP/ papillotomy is indicated. In elderly patients and those
with co-morbid diseases, a papillotomy will suffice to prevent recurrent attacks of pancreatitis.

There is no place for surgery during the early phases of severe pancreatitis, unless there is abdominal
compartment syndrome or ischemic large bowel necrosis which occurs rarely during this phase.