ANATOMY OF THE PANCREAS

• It is a gland organ of th digestive system.

• Located in the c loop of the duodenum(b/n the two flexures)
• It is a fleshy organ
• It is retroperitoneal
• It is packed in an oblique position with the head of the pancreas within the
duodenal loop
• The pancreas has a head, neck, body and tail
• The tail of the pancreas is located at the hilium of the spleen, which is also
close to the left flexure of the colon

‣ This is significant because during a splenectomy or left sided colectomy,

the tail can be injured causing iatrogenic pancreatitis.

• The average weight of the pancreas is 80g. The length is a range from about 25
to 30cm.
• Around the head of the pancreas is a downward pointing process known as the
uncinate process.
• The head and neck of the pancreas makes 30% of the weight, body and tail 70%.
• The pancreas has exocrine and endocrine functions
• The exocrine part makes up 80 to 90 % of the weight, the endocrine part
makes up 2 %, the mesenchyme makes up 8%.
• Behind the head of the pancreas
◦ IVC
◦ right renal artery and vein,
◦ and left renal vein.(the left renal vein is longer and is
displaced towards the right),
◦ body of the second lumbar vertebrae.

• NB in children, when there is a blunt trauma to the abdomen, the compression

presses on the head of the pancreas which presses on L2 causing
retroperitoneal bleeding
 i

BLOOD SUPPLY OF THE PANCREAS

Supplied by branches from the celiac trunk and SMA.
CELIAC TRUNK
Celiac trunk- splenic artery, left gastric artery and common hepatic artery.

The splenic artery supplies mainly supplies the spleen and gives off
• Branches to the spleen( pancreatic branches of the spleen)
• short branches known as the short gastric arteries or vasa brevis, which
supply the cardia
• Left gastroepiploic artery which supplies the left part of the greater
curvature of the stomach.

The left gastric artery: supplies the left part of the lesser curvature of the
stomach

Common hepatic artery: first branch is the right gastric artery which
anastomoses with the left gastric artery to supply the lesser curvature of the
stomach
Gastroduodenal artery- descends down and gives
the right gastroepiploeic artery which anastomoses with the left gastroepiploeic
artery and together supply the greater curvature of the stomach.
The gastroduodenal artery continues downwards as the superior
pancreaticoduodenal artery and passes behind the head of the duodenum.

NB: that’s why in duodenal ulcer there can be bleeding

from this artery

Once it reaches the inferior margin of the duodenum, it will split of bifurcate
into two parts;
• Anterior superior pancreaticoduodenal artery
• Posterior superior pancreaticoduodenal artery
• These parts supply the head and the neck of the pancreas.
SUPERIOR MESENTERIC ARTERY
• Located behind the neck of the pancreas
• Gives of the inferior pancreaticoduodenal artery- head and neck
• It also bifurcates and gives off two branches:
◦ Posterior inferior pancreaticoduodenal artery
◦ Anterior inferior pancreaticoduodenal artery
• These arteries go and supply the proximal 2/3 of the pancreas
• The posterior 1/3 of the pancreas will be supplied by the splenic artery.

The posterior surface of the pancreas has a groove, this groove contains the
splenic artery

The Inferior pancreatic artery also supplies the pancreas and is inferior to the
splenic artery.

Embyrologically there are two Pathologies that are common:

◦ Annular pancreas: head of the pancreas forms a ring around the duodenum
causing duodenal obstruction
◦ Pancreatic divisum: when the pancreatic head does not rotate and join the
body and tail hence there is more than one pancreatic duct.. (NB.
Embryologically Head and body develop separately)

HE t.t.si
In some people there are two pancreatic ducts in which case we have:
Duct of wirsung(main pancreatic duct)- in the head of the pancreas
and
Duct of santorini.(accessory pancreatitic duct) in the body and the neck
NB these two ducts are supposed to fuse together when the pancreas
rotates embryolocically.
Exocrine function of the pancreas
• Main cells here are the acinar cells of the pancreas.
• The pancreas has acinar cells, arranged in a cylindrical form such that there is a
central lumen.
• The acinar cells produce enzymes that are contained in the central lumen.
• The acinar cells have duct, called intercalated ducts. Thee intercalated ducts go
ahead and become interlobar ducts. These interlobar ducts fused together to
for the pancreatic duct.
Exocrine secretions of the pancreas
They are usually zymogens(inactive enzymes) which which need to be activated.

• Pancreatic Lipase
• Trypsinogen
• Pancreatic amylase
• Chymotrypsinogen
• Proelastase
• Phospholipase a2
• Procarboxypeptidase
• Dioxyribonuclease
• Ribonuclease

Hereditary pancreatitis
• This is due to a mutation in the SPINK1 gene.( serine protease inhibitor Kazal
type one) also known as pancreatic secretory trypsinogen inhibitor.
• Everyone usually has this gene working properly
• It works by inhibiting trypsinogen from activating, ie when not needed
• When there is a mutation here there is invariable activation of trypsinogen to
trypsin which causes auto digestion of the pancreas( since its technically
protein) causing pancreatitis.

ACUTE PANCREATITIS
Sudden onset inflammation of the pancreas. It may be infectious or non infection
in origin..
Etiology
Commonest cause of acute pancreatitis is alcohol followed
by gall stones. Most common cause of chronic pancreatitis
is alcohol.
I GET SMASHED
I- IDIOPATHIC OR IATROGENIC

G- GALL STONES
• The gall stone pssses through the cystic duct into the biliary duct,
occluding the ampulla of vater. Thereby blocking the exocrine
secretions from being released. They build up and cause
autodigestion of the pancreatitis

E- ETHANOL sphincter
• Causes spasms of oddi which makes it difficult for the enzymes to
come out into the gut, causing decreased drainage and premature
activation of the enzymes causing autodigestion
T-TRAUMA
• The pancreas overlies L2 and so it can easily be compressed

S-SCORPION BITE
• Particularly by tityus trinidatus( not in ghana)

M-MUMPS/MALIGNANCY

A-AUTOIMMUNE
• main thing seen is immunoglobulin G4,

S-STEROIDS

H-HYPERCALCEMIA/HYPERTRIGLYCERIDEMIA listento é explanation

 Calcium is a strong activator of enzymes.

Nb: hypocalcemia can be a complication of pancreatitis.

E- endoscopic retrograde cholangiopanreatography(ERCP) explanation

D-DRUGS
• Eg. Furosemide, tetrecycline, thiazide diuretics theseonesi use tohyperunion
whichleads to hypercalcemia

Pathogenesis
• The acinar cells contain these zymogenic granules.
• Trypsinogen is being inhibited by SPINK1
• When there is injury of the pancreas there is influx of calcium within the
acinar cells
• The calcium willl cause fusion b/n the zymogenic granules and lysozomes
• The lysozomes will activate trypsinogen within the acinar cells
• When trypsinogen is activated it becomes trypsin, and trypsin activated the
other zymogens.

‣ NB. Trypsin has an autocatalyzism activity, ie can activate itself

unlike the other zymogens

Physiologically, When food is taken, trypsin is activated by enterokinase.

• When the pancreas begins to autodigest, destroying the pancreas it is called

liquefactive necrosis

the commonest type of necrosis is coagulation necrosis.

another organ that undergoes liquefactive necrosis is the brain

The pancreas is surrounded by adipose tissue, when they dissolve the pancreas
and get to the fat tissue. they dissolve the fat cells it is called FAT NECROSIS.
This fat necrosis leads to the a phenomenom known as SAPONIFICATION.
• In the process of saponification, free fatty acid and mono glycerine should are
released. These free fatty acidic will act on serum calcium forming white flakes.
• Hence there is both liquefactive and fat necrosis in panceatittis.

◦ This is how they diminish the calcium reserves

causing hypocalcemia.

Clinical presentation
Mild form
• Severe epigastric pain- which radiates to the back.
• Relived by leaning forward(vanzant sign) Explanation

Why do they feel relived on leaning forward?

Because leaning forward displaces the pancreas from the
anterior abdominal wall and so it doesn’t irritate the
anterior abdominal wall.
• Vomiting- not preceded by nausea
• Retching
• Constipation
• Fever
• Tachycardia
• Hypocalcemia

In cases where the pancreas becomes hemorrhagic you have periumbilical and flank
pain associated with a discoloration.
Cyranohue chronic
Cullen’s sign-periumbilical
Grey turner’s sign- flank
With severe pancreatitis,
• The bowel wall can be damaged causing paralytic ileus.
• Profuse vomiting
• Severe abdominal pain
• Pleural effusion or respiratory distress
• Cyanosis
 How does it cause pleural effusion?
• This is due to elastase, which damages the lining of the pleura.
• Signs of shock- hypotension, tachycardia, cold extremities, increase capillary
refill time and decreased urine output.
• Signs of hypocalcemia

Investigations
• Serum amylase level
• Serum lipase level( more sensitive)- should be three times the upper limit
• FBC
• ultrasound scan
• abdominal CT
• ERCP(most be done carefully as it’s also a cause. Ironic innit)

PANCREATITIS SCORING SYSTEM

• Glasgow scoring system( Glasgow imrie criteria)
• Used within the first 48 hours of admission to assess the severity
• Very sensitive if it is caused by alcohol or gall stones

PANCREAS
P-PaO2 less than 8KPa
A-Age greater than 55 years
N- neutrophils. WBC > 15 x 10^9 /L
C- calcium < 2mmol/l
R- renal function ( urea >16mmol/l )
E - enzymes (LDH > 600iU/l and /or AST > 2000iU/l)
A - albumin < 32g/l
S - sugar ( glucoses > 10mmol/l )
Each has a score of one.
1- mild 2- modest. >3- severe

Risk of Mortality
0-2 -> 2% , 3-4 -> 15 , 5-6 -> 40% , 7-8 -> 100%
Ranson’s criteria

Two versions: old( used for pancreatitis caused by alcohol) ranson’s

modified (just for gall stones) ranson’s

Can be calculated at admission and at 48 hours for both criteria.

For admission(SWABS)
S- Serum lactate dehydrogenase ( should be greater t
W- WBC > 16000/mm3
A- AGE more than 55
B- blood sugar>200mg/dL
S-AST>250 iu/l

AT 48 hours(BASE BH)

B- base deficit> 4mEq/l

A- arterial pressure <60mmHg
S- serum calcium <8mg/dL
E- estimated fluid extravasation(fluid loss)> 6L
B- bUE creatinine> 5mg/dl

0-1= mild , 2= moderate, >3 = severe.

APACHE SCORING SYSTEM
• Clan be used irrespective of the cause

Nb: pancreatitis can cause multiple organ failure and for that we use a score
called the SOFA score (severity of organ failure assessment)

MANAGEMENT
• Admit the patient
• Assess airway, breathing and circulation
• Secure IV Assess and take samples for relevant labs(FBC, BUE and creatinine,
serum calcium levels, LDH levels, blood sugar, serum amylase and lipase, ABG,
urine amylase and lipase)
• Give IV fluids
• Pass a catether and monitor urine output and vitals
• Monitor spO2 and give oxygen if needed
• Pass an NG tube, but the moment the patient can tolerate food, feed to
prevent paralytic ileus
• Give adequate analgesics( codeine),only after diagnosis has been established

• NB- stay away from opioids ( morphine and Pethidine) because they
can cause spasm of the sphincter Of oddi)

• Give antibiotics if there is evidence of an infection.

Complications
Local complications
• Pancreatic abscess
• Pancreatic pseudo cyst Listento the
• Pancreatic fistula
• Pancreatic carcinoma(main cause of obstructive jaundice in adults)
• Bowel ischemia
Systemic complications
CNS: seizures, coma, purtshcer’s retinopathy( occlusion of the retinal artery due
to hyperlipedemia)
Cardiovascular: hypotension, pericardial effusion, arrthymias
Respiratory: pneumonia, atelectasis, pleural effusion,acute respiratory distress
syndrome.
Renal: acute kidney injury
Hematologic: DIC.
GIT: peritonitis, paralytic ileus,stress ulcers, splenic rupture,
Metabolic:hyperglycemia(diabetes),hypocalcemia

Differentials of pancreatitis
Any differential for acute abdomen will work here.eg
• Acute cholecystits
• Peptic ulcer
• Hepatitis
•