Pancreas

 Pancreas is the most

important and
digestive gland
involved at the same
times in the regulation
of the carbohydrate
metabolism. It has a
weight of 80-90 gr.
With gray-pink color,
consists of individual
components- lobules
and acynusis.
 Pancreas
 The pancreas is a retro-
peritoneal /in front of the spine/
at L1-L2, head-the right of them,
the body-in front of the L1, the
tail reaches the left edge of the
arc at the 9-12 ribs.
 The projection of the pancreas to
the anterior abdominal wail :the
l. median - lower edge of the
projected 5 cm. above the navel,
the upper 10 cm. above it.
 pancreas
 Pancreatic head is in a
concavity 12 duodenum.
 Processus uncinatus located
in the lower body RV.
 Neck - located between the
head and body.
 The body – located behind
the wall of the stomach
reaches lien and region of
ileo - renal ligament.
 Anatomy of the pancreas
 The length – varies from 10 – to 23 cm., thickness 2-3
cm.,maximal head height 4-5 cm.

 P. consists of parenchyma,
excretory ducts system and
connective – vascular stroma. P.
is covered by connective tissue
with septs which runs thick
gland, dividing it into segments

 80% of P. is parenchyma with a basic exocrine function /

97 – 99% by weight/ and to a lesser extent endocrine
provided islets of Langerghans /1 ml. in humans/.
 Pancreatic duct

 Duct collected pancreatic digestive juice what

leaves then in p. duct from head to teal. P. duct
is opened in duodenum from the level of
duodenal papilla, near common bile duct.
 Wirsung duct – the main pancreatic duct
 P. ducts are collected digestive juices and fed to the d.
pancreatic, pierce gland from tail to head, called in
duodenum at the level of a large duodenal papilla near d.
billiary common .

 The largest part of the

Wirsung duct /4 mm/ is in a
head of pancreas, narrowing
to 2 mm in the tail.
 Wirsung duct located near
and parallel to the common
bile duct, forming a common
before it opens in duodenum.
 The exocrine part of pancreas
 It is formed from acinar and duct
cells.
 Each acin consists of 8 – 12 acinar
cells, that secrete digestive
enzymes. Acinar cells formed acini
/looking like grapes/.
 The ducts, which secreted
bicarbonate and mucus used to
mix with enzymes. This ducts
form a netting, what excreting
content in the main and
additional ducts open into the
duodenum.

Endocrine pancreas
The cells of the endocrine
cells
system /4 types/ are
organized in the islets of
Langerghans, which secrete
hormones that regulate blood
sugar levels.
  -cells (insulocytes bazofili/
are 50 – 80% of the insular
masses, located in the center
of the islets secrete insulin
and amylin.
- cells (insulocytes acidofili) are 5 – 20% of the mass of
islands, located on the periphery islets secrete glucagon.
 Endocrine system cells
  -cells (insulocite definitive) account for 5% of the
insular masses, are on the periphery of the islets,
secrete somatostatin and, possibly gastrin.

 PP-cells constitute 10 –
35% of insular masses,
but aren’t in the islets,
and exocrine pancreas .
These cells secrete
pancreatic polypeptide.
 Histology of the pancreas
 Cells with lowering
color – Langherhans
isllets. Cells with hight
color – acini cells, that
are connected with
ducts and secrete
digestive enzymes into
the intestine. Color with hematoxilin and eozina
1 - gland acini
2 - islets Langerhans
3 - principal duct
4 – interlobular duct
5 -interlobular tissue
 Histology of pancreas

Color with hematoxilin and eozin
1 - аcini
2 - Langherhans islets
3 - interlobular tissuie
4 – vessels
Color with hematoxilin and eozin
1 - аcini
2 - Langhergans islets
3 – interlobular duct
4 - interlobular tissuie
 Physiology of the exocrine pancreas
Function of pancreas – exo- and endogen secretion

1.intracavitary
intestinal digestion by
enzymes of acini cellls

2. Support of intracavitary
in the intestine in neutral leve
lev

Endocrine function regulates

Carbohydrate metabolism and
Utilization of cellular products
Of digestion in the body
 Pancreatic endocrine function

 Insulin ( - cells) provides

penetration of glucose and
other nutritients from the
blood into cells. With an
increase in blood glucose,
its utilization provides
tissue for energy.
 Pancreatic endocrine function

 Glucagon promotes
the breakdown in the
liver and glucogenes
in the blood, when its
level falls bellow the
acceptable normal
range.
Pancreas during the day secretes 1-1,5 liters of
pancreatic juice /clear, viscous liquid, the weight of
1998-1012, pH 7-9.

The juice contains 7-10% of protein, of which the most

important enzymes and proenzymes is, the rest is the
content of the plasma contains mucoprotein trypsin
inhibitors.

In acinar cells is synthesized and deposited in the

granules of all pancreatic enzymes, but in different
proportions.

Protease and phospholipase synthesized in an inactive

form of amylase, nuclease secreted in active form.
 Water and electrolytes
>> Pancreatic
Pancreatic electrolytes
electrolytes secreted
secreted alkaline
alkaline medium
medium
isoosmotic
isoosmotic with
with the
the extracellular
extracellular fluid.
fluid.
The
The main
main cations
cations Na+Na+ and
and K+,
K+, are
are secreted
secreted atat aa
concentration
concentration similar
similar toto that
that in
in aa similar
similar plasma
plasma
concentration
concentration isis independent
independent of of the
the secretion
secretion
capacity.
capacity.
Major
Major anions
anions HCO3-
HCO3- and and Cl-,
Cl-, their
their concentration
concentration
is
is determined
determined byby the
the secretion
secretion capacity.
capacity.
With
With the
the increase
increase of of the
the secretory
secretory capacity
capacity of of
bicarbonate
bicarbonate concentration
concentration rises rises to to aa plateau
plateau
level
level of
of 150
150 mEq/l
mEq/l andand Cl-Cl- level
level is is reduced,
reduced,
that
that is
is the
the sum
sum of of anions
anions equal
equal to to of
of cations.
cations.
 Water and electrolytes
Water
Water diffunded
diffunded into
into pancreatic
pancreatic juice
juice passively,
passively,
according
according to to the
the osmotic
osmotic gradient
gradient established
established by by
active
active secretion
secretion of of electrolytes
electrolytes and
and other
other soluble
soluble
substanses.
substanses.
Bicarbonates
Bicarbonates -- their
their secretion
secretion is
is ensuring
ensuring withwith
carbonic
carbonic anhydrase
anhydrase of of ductal
ductal cells.
cells. ItIt affects
affects
blood
blood and
and interstitial
interstitial cells
cells CO2
CO2 due
due to to passive
passive
diffusion,
diffusion, allowing
allowing thethe formation
formation ofof carboxylic
carboxylic
acids.
acids.
Pancreatic
Pancreatic juice
juice also
also contain
contain Zn,
Zn, Ca,
Ca, Mg,Mg,
HPO42-,
HPO42-, SO42-.
SO42-.
 Regulation of pancreatic
secretion
Hormone
Peptydergic system Coletsistochinin
Galanin Secretin
Peptid of free of gastrin Gastrin
Substanse P Vombezin
Neuropeptid Neurotenzin
Peptid of gene of
Pancreatic secretion Hormone of
caltsitonin Parathyroidal gland
Peptid hystidin-izoleitsin

Pancreatic polypeptid
Polypeptid GG
Somatostatin
Glucagon
Caltsytonin
vasopressin
 Phases of pancreatic secretion
In pancreatic secretion there are bazal secretion in
time of taken meal and after

Basal secretion

 Before to the meal – the enzyme secretory

function is minimal.

 After meal – secretory activity increases by 60-120

min.
 Phases of pancreatic secretion after meal
Phase secrety stimulation Мechanisme

Cerebral 25% Look, smell, taste, Vagus, vagoentering:

swallow Gastrin - blood

Stomach 10% Dilatation of Vago - vagus

Stomach, protein,
Amino.

Intestinal 50-75% Аmino Coletsistochinine,

Lypoprotein, Secretine,
Ca, dilatation Enteropancreatic,
Colinergic reflexes
B. Methods for studying enzymes in duodenal contents by 2-
channel special probe

This method revealed the following types of dysfunction

of pancreatic secretion

1.Hyposecretion– decrease of 2. Hypersecretion – increase of

enzyme secretion and enzyme activity, volum is normal
dicarbonate in normal volume

3. Obstructive type identifies two types of blocks: hight – normal

consentration of bicarbonate, decrease volume of secretion, but increase
increase activity of enzymes; lower – decrease volume of secretion with
normal concentration bicarbonates

4. Ductal – decrease volume of secretion, increase concentration of

bicarbonate and normal level of pancreatic enzyme
C. Tests determining the activity of enzymes in pancreas

o Тest the NBT – PABA /bendiromid/. Number

PABO urinary excretion reflects the activity of
chimotrypsin. Sensibility of 80 -90%
C. Тests determining the activity of digestive pancreatic

o Тest with H-pancreolanurine – determined the

activity of colesteril esterase. Sensitivity of 90%.
Specificity 97%.
o Silling test – reflects malabsorbtion of Vit. B 12,
with using two radioactive markers.
o Respiratory test – with cholesteryl-13C-
octaonatom.
 Determination of the concentration of enzymes in fecales

Determination elastasae -1 in stool (ELISA).

Norm: 200-500 µg/g feces at failure - <200 µg/g/ The
sensitivity 90%.

 Determination chimotrypsine in the stool(ELISA):

norm -290 mcg/g. inssuficiency - < 90 mcg/g.

 Coprograma:gray color,in normal volum. In the

initial stage of insuficience – steatorrhea, then –
creatorrhea, then – amilorrhea /amidonum/.
 D. Determination of endocrine function of
pancreas
 Determination of glucose-tolerance test.
 Glucose profile
 Glucosuria
 Determination of insulin, C-peptide.
 Instrumental methods of diagnostic of
pancreatic disease

Survey radiography
of the abdomen:
intraduct
calcifications, less
fabric in the pancreas
R-graphy with
bariumsulphate
reveals dilatation of
retrogastric space Radiografia abdominală arată
calcificarea difuză
and a horseshoe of
duodenum
 Instrumental methods of diagnostic of
pancreatic disease

Ultrasound in chronic pancreatitis: dilatation of Wirsung

duct >3mm, cyst >1cm., calcifications, heterogeneity of
the parenchyma resizing the pancreas.
Echoendoscopy – heterogeneity of parenchyma, duct
dilatation >3mmin the head region and >1mm in the
region of tail, see additional branches of the main
pancreatic duct
 Computed tomography
 More sensitive method
than abdominal
sonography, reveals the
ducts dilatation, cysts,
calcifications.
 The method is valuable
differentiating the
diagnosis of chronic
pancreatitis and
pancreatic tumors Scanare prin CT demonstrează
pancreatita cronică
 Classification of chronic pancreatitis /according to CT
dates/
The normal pattern
The main pancreatic duct 2mm.
Size, shape – normal
Normal parenchyma
Doubtful diagnosis
One of the following symptoms:
Wirsung duct 2-4mm
Mild hypertrophy >2-fold above
normal
Heterogeneous parenchyma
Mild form
2 symptoms –
Wirsung duct 204mm.
Mild hypertrophy >2
The average weijht
Cysts <10mm.
Irregular ducts
Acute focal pancreatites
Increased echogenicity of the
walls of ducts
Irregular contour of the
pancreas
Severe form
Any of the above symptoms
plus one of the following:
10mm cyst
Defects intraduct filling
Stones, stenoses of ducts
Loss of adiacent organs
 Retrograd cholangiopancreatography with
useing RMN /MRCP/
 This method is used then CT
unshowed pathology.
 This method has the
advantage that irradiation
does not apply, do not use
intravenous contrast.MRCP
visualize bile ducts and
pancreas.

MRCP demonstrează pancreatita

cronică
 Endoscopic RCP /ERCP/

 ERCP – visualized bile duct and pancreatic ducts during

duodenoscopy with intoduction of special contrast, that is
visibile at R-graphy.At the same times visibile during endoscopy
duodenum and duodenal papilla.
 In patients with mild chronic pancreatitis diagnostic
value of ERCP low as it can identify only the minimal
extension of the main pancreatic duct and of its
branches.
At moderate chronic pancreatitis pancreatic duct
extension of the basic > 2,5 times more than the norm,
the formation of of rouded extension of its branches.
 Severe form –significant dilatation
of main pancreatic duct /such sa
lakes/, more than > 1,5
 The side branch duct greatly
expanded, forming stones in the
pancreatic ducts, with ther
occlusion. Pancreas condensed,
changing its color gray-yellow
color.
 ERCP – Cambridge classification
Norm
 Normal pancreatic duct
 Its branches is unchange
Doubtful diagnostic
 Normal pancreatic duct
 1/3 of branches is changed
Mild form
 Normal pancreatic duct
 3 of branches is changed
The average weight
 The main pancreatic duct is
changed
 >3 branches are changed
Several form:
One of the above changes + 1 or
more symptoms:
 cavity > 10 mm
 Stones, finding defects in the
duct
 Stenosis, lesions of adiacent
organs
 Chronic pancreatitis /CP/
CP
CP–the
–thecharacteristic
characteristicinflammation
inflammationof ofpancreas
pancreas
characterized
characterizedbybyirreversible
irreversiblemorphological
morphological
changes
changesininappearance
appearanceand andin
inthe
thesecretory
secretory
function
functionof
ofthe
thepancreas
pancreaswith withspecific
specificpain
pain
syndromes
syndromes and andororsymptoms
symptomsof ofpancreatic
pancreatic
insufficiency.
insufficiency.
 Morphology

Figura 1 ţesut pancreatic normal figura 2 Pancreatita cronică: fibroza densă

 Chronic pancreatitis is characterized by three main

features: inflammation, fibrosis and atrophy of gland.
 The chronic inflammation induced sclerosis, the loss
of functionally active parenchyma and disturbanses
of normal sructure of organ.
 Epidemiology
Incidence –– 8,2
Incidence 8,2 new
new cases
cases per
per 100.000
100.000
inhabitants/year /Europe/.
inhabitants/year /Europe/.
The total
The total number
number of of patients
patients –– 26.4
26.4 cases/year
cases/year /Europe/,
/Europe/,
≈≈ 20
20000
000 in
in Germany
Germany ;; ≈≈ 60 60000
000 in
in Russia
Russia ;; 126/100.000
126/100.000 in in
India.
India.
Frequency -- 6.7
Frequency 6.7 in
in men
men and
and 3.2
3.2 // 100000
100000 in in women
women..
CP more
CP more found
found in in men
men 45-54
45-54 year,
year, after
after which
which there
there isis aa
decrease of
decrease of number.
number.
In women
In women thethe frequency
frequency remain
remain equal.
equal.
Among men,
Among men, most
most often
often caused
caused by by CP
CPisis alcohol,
alcohol, women
women
–– hyperlipidemia.
hyperlipidemia.
Race: In
Race: In african-americans
african-americans found found 33 times
times more
more often
often
than among
than among caucasian
caucasian race.
race.
 Etiology.Causes of CP /system TIGAR-O+/
А. Тoxico-metabolic
•Аlcohol
•Smoking
•Hipercalciemia
•Hiperlypoproteinemia
•Chronic renal failure
•Drugs and toxins
•Idiopathic
•Тropical
D. Autoimmune
•Isolated pancreatitis
•Bind with other autoimmune
diseases: S. Sjogren, billiary
cirrhosis
•Inflammatory bowel disease
B. Genetic
•Аutosominduced /trypsinogen gene mutation/
•Recesive autosomal transmition /gene SPINK
1, CFTR, trypsinogen cat, cod 16, 22, 23, a-1
antitrypsin deficiency/
C. Оbstructive
•Оbstraction of the ducts/tumor/
•Stenosis
•Pancreas “Divisum”
•Dysfunction of the sphincter Oddi
E. Acute several relapse pancreatitis:
Severe acute necrotic pancreatitis
Acute relapse pancreatitis
Radiation
Ischemia
 CP and alcohol

Alcohol in 70% of causes induced the

development of CP in male 30-40 years
old who using alcohol in dose of 20 g/day
for 6-12 years.
 CP and alcohol

 Аlcohol affects the pancreas as follows:

 a) in the initial stage is develop perilobular fibrosis than intralobular
fibrosis ;
 b) the presence of protein droplets in the ducts what obturate it;
 c) dilatation of intralobular ducts;
 d) loss of functional part of pancreas, lobular atrophy. In the altered
lobules the most typical pattern – variable number of advanced of
acini and ducts.
 CP and abnormal development
“Pancreas divisum “

 “Pancreas Divisum” - there is – 10% of patients as a result of

incomplete fusion of the dorsal dorsal ducts during
embriological development. D. Wirsung empties in duodenum ,
but drains only a small portion of pancreas /ventral part/ . Other
regions /tail, body, neck/ , and the remainder of the head drain
through the minor papilla via the duct Santorini.
 Оbstructive pancreatitis
 - is associated with obstruction of the secondary
pancreatic ducts and structures resulting of the
inflammation or tumors /benign or malignant/
 Another cause of obstructive pancreatitis is
dysfunction of sphincter Oddi, the presents os
stouns, intraductal erosies, dilatation of distal
duct – to it obstruction.
 Hereditary CP
 - manifests itself in childhood, usually between 10-12
years. Transmission – by dominant autosomal gene
with incomplete penetration.
 There is one of the two mutations /R122H or N291/ gene
of trypsinogen./gene PRSS1/.
 - is characterized by recurrent episodes of pain.
Diabetes in these patients is appear in 20% after 8-10
years of debut of pain. This form is complicated with
tumor.
 The pathogenesis of CP
Increasing of pancreatic secretion /alcohol,
drugs, food/
Disturbances of the pancreatic secretion in
duodenum /pathology of Vater amp., increasing
the pressure in the duodenum/.
Intra-pancreatic activity of the enzymes in
pancreatic tissue damage.
The circulation of active pancreatic enzymes in
the blood.
Progressive atrophy of pancreas and appearing
of pancreatic insufficiensy /exo- and endo-
parts/.
 Pathogenesis of CP
Тheory of the
“small ducts” Neuroimmune theory
The beginning of disease is (with warmly of T-sup., cytokines
Associated with small streams acini what influence autoimmune
where are formed containing processes)
eosinophils precipitates and
than stones.

Chronic pancreatitis

Theory of primary lesion

Acini with toxic metabolites
Necrosis – fibrosis theory
and oxidative stress.
 Chronic pancreatitis
 Different pathogenic factors
caused chronic inflammation
pancreas then fibrosis and
stricture of ducts, who disturb
intra-pancreatic function of the
pancreas, induced irreversible
and progressive histologic
changes.
 In contrast to acute pancreatitis
CP is characterized by relapse
and persistent clinic and
laboratory symptoms.
Classification of CP /WHO, 10th revision/
K 86.0 CP alcohol etiology
K 86.1 Other CP
with recurrence
recidivante
infectious
K 86.2 cysts of pancreas
K 86.3 pseudo-cysts of pancreas
K 86.8 other diseases of the pancreas
Atrophy
Stones
Cirrhosis
Fibrosis
Necrosis
Aseptic
Adipose
Infantilism of the pancreas
K 86.9 unrefined disease of the pancreas
 Classification M-ANNHEIM of the CP
/conform risk factors /
 Pancreatitis
 The use of alcohol:
 • excessive (> 80 gr/day).
 • high(20-80 gr/day).
 • moderate (< 20 gr/day).
 The use of nicotine:
 • the number of packets/year.
 Nutritional factors:
 • with much use of fat and protein.
 • hiperlipid emia.
 Classification M-ANNHEIM of CP /conform
risk factors/
 Changes in efferent pancreatic duct:
 • Pancreas “Divisum”.
 • Circular pancreas and other genetic abnormalities .
 • Obstruction of the pancreatic duct.
 • Post – traumatic stricture of pancreatic duct.
 • Sfincter of Oddi disfunction.
 Immunological factors:
 • Autoimmune pancreatitis.
 • Sjogren syndrome associated with CP.
 • Bowel diseases, PBC associated with CP
 Other rare factors:
 • Hyper-para thyreoidism and hyper-calciemia.
 • Chronic kidney failure.
 • Drugs.
 • Toxins.
 The main clinical syndromes of CP

I. Pain syndrome.
II. Endocrine syndrome.
III. Exocrine pancreatic insufficiency.
IV. Dyspeptic syndrome.
V. Allergy syndrome.
 I. Pain syndrome
 Pain is manifested in the epigastrium
hypo-condrium, often in left, which
may be of different intensities,
periodic, recurrent or permanent,
may be without pain within CP.
 Irradiation of pain is different, may be
in the spine, lumbar /L2/,the chest.
Pain is relieve in Bozeman’s position,
using spasms and cholinolytics .
 Clinic
The intensity of pain may be
hight in unagreement with
Pain is situated in epigastrium, left absence another clinic
hypocondrium and lower of novel symptoms.

Irradiation of pain in left Pain is relieve in

hypocondrium , in spine, Bozeman’s position
Intra-scapular area.

Pain is characterized with 24 hour Is present contact of pain

duration may be intermitent with with fat, pungent fast. Pain
light periods. decrease in hungry .
The causes of abdominal pain in CP.
 Inflamation of
Inflamation of the
the pancreas
pancreas tissue
tissue /nerve
/nerve
compression, tension
compression, tension capsules/
capsules/
Complications::
 Complications
Intra-pancreatic: obstruction
 Intra-pancreatic: obstruction of of the
the ducts,
ducts,
pseudocysts, pancreatic
pseudocysts, pancreatic neuritis.
neuritis.
Extra-hepatic: stenosis
 Extra-hepatic: stenosis ofof intra
intra pancreatic
pancreatic part
part
of coledoch,
of coledoch, duodenum
duodenum stenosis.
stenosis.
Syndrome exocrine
 Syndrome exocrine pancreatic
pancreatic insufficiency:
insufficiency:
flatulense with
flatulense with increased
increased intra-bowel
intra-bowel pression,
pression,
impaired motor
impaired motor function,
function, intestinal
intestinal bacterial
bacterial
overgrowth.
overgrowth.
Diseases associated
 Diseases associated withwith the
the pathology
pathology ofof the
the
gastro –intestinal
gastro –intestinal tract.
tract.
 II. Endocrine syndrome

 In
In the
the early
early effects
effects ofof hyper-insulinisme
hyper-insulinisme may may be be aa
phenomen
phenomen occursoccurs hypo-glykemia
hypo-glykemia than than associated
associated
failure
failure of
of the
the endocrine
endocrine function
function of of the
the pancreas
pancreas::
-- Disturb
Disturb ofof the
the test
test for
for glucose
glucose tolerance
tolerance
-- Transient
Transient diabetes,
diabetes, whatwhat appearing
appearing during
during the
the
period
period ofof acute
acute pain
pain
-- Diabetes
Diabetes as as the
the first
first sign
sign of
of CP
CP
-- Diabetes
Diabetes whatwhat appearance
appearance in in complications
complications of of CP
CP
-- Diabetes
Diabetes whatwhat appeared
appeared in in later
later stages
stages ,, till
till 10-20
10-20
years
years ofof present
present CP CP
 III.Exocrine insufficiency
 This
This syndrom
syndrom appears
appears along
along with
with the
the
progression
progression of
of CP
CP and
and with
with the
the following
following
symptoms
symptoms::
a)
a) Mal-digestion
Mal-digestion and
and mal-absorbtion
mal-absorbtion
 Mal-digestion
Mal-digestion syndrome
syndrome –– disturbances
disturbances of
of
digestion
digestion in
in the
the cavity
cavity of
of thin
thin intestine
intestine
 Mal-absorbtion
Mal-absorbtion syndrome
syndrome –– appear
appear at
at
late
late stages
stages ofof CP,
CP, when
when thethe function
function of
of
exocrine
exocrine pancreas
pancreas decrease
decrease in in more
more
than
than 90%.
90%.
 III.Exocrine insufficiency

 In
In both
both syndromes
syndromes there
there are
are diarrhea,
diarrhea, polyfecales
polyfecales
/steatorreya,kreatorea,
/steatorreya,kreatorea, amylorrea/,
amylorrea/, weight
weight loss,
loss,
dry
dry skin,
skin, mucous
mucous membranes,
membranes,
hypoavitaminousis.
hypoavitaminousis.
 In
 In mal-absorbtion
mal-absorbtion syndrom
syndrom assosiated
assosiated anemia
anemia
/B12/.
/B12/. Is
Is disturbances
disturbances protein
protein changes,
changes, gastro-
gastro-
intestinal
intestinal hormones
hormones secretion,
secretion, there
there are
are the
the
fatigue,
fatigue, weakness,
weakness, depression,
depression, sleep
sleep
disturbances.
disturbances.
 IV. Dyspeptic syndrome

 Dyspeptic
Dyspeptic syndrome
syndrome manifest
manifest discomfort
discomfort inin the
the
abdomen,
abdomen, intolerance
intolerance to
to fatty
fatty food,
food, belching
belching air,
air,
food,
food, loss
loss of
of appetite,
appetite, hypersalivation,
hypersalivation, nausea,
nausea,
vomiting,
vomiting, which
which does
does not
not bring
bring relief,
relief, swelling,
swelling,
unstabile
unstabile fecales
fecales /constipation,
/constipation, diarrhea
diarrhea change/
change/
and
and diarrhea.
diarrhea.

V
V.. In
In 30-35%
30-35% of
of causes
causes there
there is
is aa food
food or
or drug
drug
allergy.
allergy.
-- Pain
Pain recurs
recurs occurs
occurs inin 90%
90% causes.
causes.
-- Mal-absorbtion
Mal-absorbtion syndrome
syndrome –– in
in CP
CP >5years-65%,
>5years-65%,
>10years
>10years –– in
in 95%.
95%.
-- Disturbances
Disturbances of of carbohydrate
carbohydrate metabolism
metabolism –– in
in 30%
30%
The examination of the patient with
CP
The
The skin
skin may
may be be dry,
dry, dirty-gray
dirty-gray color
color or
or aa pale,
pale,
follicle
follicle hyperkeratosis,
hyperkeratosis, hyperpigmentation
hyperpigmentation in in
region
region ofof pancreas
pancreas /s-m
/s-m Barteeheimer/,
Barteeheimer/, in in face
face
the
the and
and limbs,
limbs, on
on the
the left
left side
side of of the
the abdomen
abdomen /s- /s-
m
m Culen/,
Culen/, atat the
the navel
navel /s-m
/s-m Turner/.
Turner/. Usually
Usually
hyperpigmentayion
hyperpigmentayion appearsappears in in the
the aggravate
aggravate of of
chronic
chronic pancreatitis
pancreatitis and
and itit lasts
lasts long
long in
in aa partial
partial
remission,
remission, disappears
disappears inin complete
complete remission.
remission.
 The red drops of Tujilin
-- The
The red
red drops
drops syndrome
syndrome –– small small size
size of
of 1-3
1-3 mm.
mm.
in
in diameter,
diameter, slightly
slightly protrude
protrude from from the
the skin
skin doesn’t
doesn’t
disappear
disappear whenwhen pressure
pressure is is applied
applied /the
/the chest,
chest,
abdomen/.
abdomen/. Hair Hair is
is brittle,
brittle, falling.
falling. Tongue
Tongue is is dry,
dry,
coated,
coated, there
there is
is bad
bad breath,
breath, maymay be be atrophy
atrophy of of
the
the tongue
tongue papillae,
papillae, fissures,
fissures, ulcers
ulcers at
at the
the corners
corners
of
of the
the mouth,
mouth, sores
sores inin the
the mouth.
mouth. The The abdomen
abdomen is is
swollen,
swollen, we we observed
observed the the atrophy
atrophy of of
subcutaneous
subcutaneous adipose
adipose tissue
tissue /Grett
/Grett s-m/.
s-m/. In
In the
the
later
later stages
stages ofof CP
CP wewe founded
founded depletion
depletion andand
protein
protein free
free edema.
edema.
Abdominal palpation revealed painful areas
and points:

 Dejarden
Dejarden point
point –– onon the
the line
line joining
joining the
the navel
navel to to the
the right
right
axillary
axillary region
region /6 /6 cm.
cm. above
above thethe navel/
navel/

 Choledoch
Choledoch –pancreatic
–pancreatic zone zone /Chauffard/
/Chauffard/ in in the
the upper
upper
right
right square
square of of the
the abdomen
abdomen /between
/between the the vertical
vertical line
line
running
running throught
throught the the navel
navel and
and the
the bissector
bissector of of the
the angle/,
angle/,
formed
formed byby aa vertical
vertical and
and horizontal
horizontal lineline going
going through
through the the
navel.
navel.

 Gubergrits
Gubergrits zonezone –– symmetric
symmetric of of the
the Soffar
Soffar zone
zone ,, but
but
situated
situated toto the
the left
left of
of midline
midline

 Gubergrits
Gubergrits point
point –– symmetric
symmetric Dejarden
Dejarden point,
point, but
but isis
located
located toto the
the left.
left.

 Katcha
Katcha point
point –– skin
skin hyperestesia
hyperestesia in in the
the left
left upper
upper quadrant
quadrant
corresponds
corresponds to to the
the innervation
innervation of of the
the chest
chest segments
segments 8-9. 8-9.

 Mayo-Robson
Mayo-Robson zone zone –– rib-spine
rib-spine angle
angle to to the
the left
left

 Palpation
Palpation of of the
the abdomen
abdomen reveals
reveals painpain inin the
the epigastrium,
epigastrium,
left
left hypochondrium,
hypochondrium, in in the
the proection
proection of of pancreas.
pancreas.
 Additional clinical signs of CP
-- Bulging
Bulging in
in the
the epigastrium
epigastrium
-- Hyperlipidemia
Hyperlipidemia promotes
promotes the
the formation
formation of
of
xanthene
xanthene
-- Weight
Weight loss
loss
-- Signs
Signs of
of hypo
hypo -- avitaminosis
avitaminosis
 Clinical forms
Alcoholic CP – 30-60% among patients with CP the ratio m/f is
2-2,5: 1, age 20-40 years. Occurs when the daily alcohol
consumption of 50-80gr./day for 18 years-men and 11 years
women. This is a primary hyperenzimatic type with
dominated pain and malabsorbtion.
Nonalcoholic CP with the destruction of ducts
In10-30% of patients with CP, the sex isn`t affected. There are
two types:
o A. Juvenile – 19 years, is characterized by pain that will
eventually subside. Progresses slowly to the development of
exocrine insufficiency and calcifications.
o B. Elderly – the age of 56 years, without any pain – 54%.
Diabetes occurs in the later stage after the development of
exocrine pancreatic insufficiency.
 Clinical forms
Hereditary CP
o Occurs in families with the presence in the ducts of
hereditary forms of CP
o Clinically mild symptoms or syndroms of acute pancreatic
attacks and steatorees.
o Frequently is detected pancreatic stones on ultrasonography
or CT.
Autoimmune
Autoimmune CP CP
oo Clinically mild symptoms or of acute attacks of
Clinically mild symptoms or of acute attacks of
the
the pancreatitis.
pancreatitis.
oo The absence of calcifications in the pancreas.
The absence of calcifications in the pancreas.
oo Determined the increase of gamma-globulin and
Determined the increase of gamma-globulin and
IgG
IgG
oo Note the increased levels of autoantibodes
Note the increased levels of autoantibodes
/carbonic
/carbonic antianhydrase,
antianhydrase, antilactoferine,
antilactoferine,
antinuclear,
antinuclear, rheumatoid
rheumatoid factor,
factor, muscle
muscle
antibodies/.
antibodies/.
oo The combination with other autoimmune
The combination with other autoimmune
diseases
diseases /PBC,
/PBC, Sjogren`s
Sjogren`s syndrome,
syndrome, Crohn`s
Crohn`s
disease/
disease/
oo Increase the size of the pancreas.
Increase the size of the pancreas.
oo Morfologically – lymphocytic infiltrate around the
Morfologically – lymphocytic infiltrate around the
pancreatic
pancreatic ducts,
ducts, fibrosis.
fibrosis.
Tropical
Tropical CP
CP
 ItItisischaracterized
characterizedby byrecurrent
recurrentattacks
attacksof ofsevere
severepainpain
arising
arisingfromfrom his
hischildhood,
childhood,lasting
lastinghours
hours–days,
–days,increase
increase
after
aftermeals,
meals,often
ofteninincombination
combinationwithwithaasevere
severeform
form of
of
diabete,
diabete,episodes
episodesof of hypoglycemia
hypoglycemiabut but rarely
rarelywith
with
ketoacidosis.
ketoacidosis.
 Frecvently
Frecventlydisease
diseaseoccurs
occursininmen,
men,very veryoften
often results
resultsinin
death
death/untreated/
/untreated/ in
in the
theprime
prime of
of life.
life.

Chronic
Chronic obstructive
obstructive pancreatitis
pancreatitis /stenosis
/stenosis of
of
papilla,
papilla, Cr
Cr pancreas,
pancreas, diverticles/
diverticles/
 ItItisiscaracterized
caracterizedby
by improved
improvedafterafter elimination
eliminationofof cause
cause,,
regresses
regressesextension
extensionduct
duct pancreas,
pancreas, reduced
reduced sings
sings ofof
exocrine
exocrinepancreatic
pancreaticinsufficiency.
insufficiency.
 Fibrosis
Fibrosisregresses
regressesasasthethedominant
dominantfaction
factionof
ofcollagen
collagen
with
withaasmall
smalllength
lengthof
oflife
life/fibronectin,
/fibronectin, lamin
lamin
procollagen3,
procollagen3, collagen
collagen3/. 3/.
Conformly of functional particulates of
CP there are 2 types Hypoenzymatic

– is appeared in last stadies CP

Hyperenzymatic – predominated parenchyma
Predominated autolise fibrosis and athophy of acini
pancreas, destruction of acini cells.
cells, edema, inflamatory
infiltration of pancreas, over >
enzymes in blood, with
decrease level in pancreatic
ducts and duodenum. Is
characterized from initial
stadies of CP.
Symptoms Hyperenzymatic type Hypoenzimatic type

Pain Intensive – with attacks, Moderate, longest.

relieve- hunger

Eczocrine Small expresive, only in Predominated in last stadies,

insufficience aggravation progressed to kahexsy

Intoxication Expresive Non-characteristic

Anamnese Short /3-5 years/ Longest />10 years/
Blood analysis increase white cells, Decrease erythrosites,
leucosites
Pancrearic Deviation phenomenon, Enzymes decrease in blood
enzymes in blood increase of enzymes level
Endocrhin Only in recidive There are permanently
disturbanses
USG, CT, RMN Edema, inflamatory Increase echogenity of
infiltration, increase of tissues, calcinates, decrease
pancreas and lymphatic of sizes
knots
 Complication of CP
Early
Obstruction of eliminatory system : pseudocysts , cysts
Vascular complication:
Global or secretory/thrombosis v. portae, v. lienalis/,
pseudoaneurisma,necrosis of adicent organ

Latest
oMaldigestion, malabsorption
oEnzyme serositis: ascites, pleurisy, pericarditis
oFat metabolic necrosis
oPancreatic diabetes, Cr of pancreas
oCompression and stenosis of the adiacent organs:
stomach, duodenum, intestines, kidneys, urinary tract.
oAnemia
oEncephalopathy
oOsteomalasy and necrosis of the femoral head
oSecunary immunodeficiency
 The evolution of CP
There are 3 stages in the course of CP:
I.Latent or subclinical with histological changes
and possible changes in the functional and/or
ultrasound, CT, RMN.

II.Stage of CP with permanent presence of pain

or with episodes.

III.Stages of failure and complication of exo and

endocrine function of pancreas.
 Treatment of CP. The problem
 Delete triggers /alcohol, drugs,
smoking, stones in biliary tract./
 Elimination of pain.

 The regulation of digestive function

of pancreas.
 Diet in CP
 Excluding alcohol, coffe, spices, fatty and
fried foods, which in cause of disturbances in
eliminatory system of pancreas, which leads
to the expansion of the ducts and the
appearance of pain .
 Reduce the number of rude and crude fiber
in relation to the effect of dietary fiber on food
enzymes /apsorbtion, requstration of
enzymes in the gel formed by the fibers/.
 Treatment of pain in CP
Problem
To reduce pancreatic secretion
Restore transit of pancreatic secretion

Antioxidans
Analgesics (Vit. A,E,C,K,Se)
NSAID Antideprisantes
Treatment of enzymes Tricyclic- amitriptilines
The suppression of secretion: Removal of obstruction
•H2-blockers pancreatic ducts
•Inhibitors of proton pump •Endoscopic procedures
•Оctreotide •Surgical treatment
•Аntiacides (drainage, resection)
Denervation of the pancreas
WHO recommendations for treatment of pain in
CP
Stage I :
1. exclude alcohol
2. diet
3. enzymes

Stage II :
1. antispasmodics
2. Analgesics – NSAID
3. Combination analgesics (codeine phosphate + paracetamol,
thricyclic phenothiazine derivates + antideprisanty )

Stage III :
1. Centrally acting analgesics / pentazocine, fortran,
tramadol /
2. Combination with psychotropic, antispasmodics /
А. From the analgesics
o Metalizol sodium /Algocalmin/ /500 mg., tab. 250-2-3 times
per day after meals/
o Tramadol /50 mg .in tab. But not more than 400 mg per day/
o Pentazocine /fortral/ - a solution of 30 mg./ml

NSAID
o Paracetamol 500 mg. (2 tab. 2 times/day )
o Solpadein – 1 tab. contains 500 paracetamol + codeine
phosphate 8mg. and 30mg. of coffeine (2 tab. 3 times/day ),
o Voltaren (amp. 3ml./day ), Nimesil
o Кetanov (amp. 30 mg./ml 1 per day)
o Acetaminophen (325 -500 mg 2-3 tab./day )

В. Antispasmodics
In 60-70% patients with CP is combined with chronic
cholecystitis, cholangitis, billiary stouns.
 Use of antispasmodics:
М-anticholinergics
.natural (atropine, platiphylline)
 synthetic
 central – aprofen, adefinin
 peripheric – Buscopan – 1t – 19ml, metamtisin /M1,3 /,
Gastrosepin /M1/
Мyotropic
 Sodium channel blockers: /Duspatalin – 200mg – 1 tab./
 Ca channel blockers – dicitel /1 tab. – 50mg/

Phosphodiesterase inhibitors: Drotaverinum – 1 tab. 0.04,

papaverine 2% - 2ml.
Nitrates
Other antispasmodics: meteospasmil, odeston, gimecromon,
diprofen, gangleron and other.
Treatment of CP – enzymes to reduce the pain

 Recommended enzymes with a high content of

proteases (trypsin) but which didn’t contain
extracts of bile and gastric mucosa. .
 Preferably in tab. (150-300 mg. 4-5 times or
more between the intake of food) – coated shell
acide resisting.
 These drugs have an effect only with
antisecretory drugs: H2 – blockers, antacids
H2 histamine receptors blockers
 Prescribed to reduce the release of secretin
duodenal mucosa of duodenum – induced
gastric acid secretion, which stimulates the
exocrine pancreas activity.
H2 blockers did pressure over
adenilatcylasae of pancreatic cells ,
reducing the synthesis of pancreatic
enzymes (famotidini, nizatidini).
 Proton pump inhibitors (PPI)

PPI inhibit secretion of HCl with the wall

cells of stomach
Decrease the acidity in the cavity of
duodenum
Decrease the secretion enzymes of
pancreas, bicarbonate and water
Omeprazole, Pantoprozole,
Rabeprozole, Ezomeprazole
Оcteotrid (Sandostatin) – a synthetic
analogue of somatostatin
• Somatostatin inhibits the flow of Ca ions in the
cells of pancreas, reducing their activity,
promoting peace functional of pancreas .
• Somatostatin improves microcirculation in the
pancreas, inhibits the secretion of the
pancreas..
• A dose of 200 mg octeotrid reduced pain in
66% of patients.
 Alternative methods of pain management
at CP
Аntienzymes drugs (contrical, trasilol, gordox )
 Assign a period of acute attack of CP at hyperenzymes
type. Effective only in the first 2-3 days of relapse.
 Have effect only in combination with antacids,
antisecretory drugs, enzymes and antispasmodics.
Аntibiotics (aminopenicillines, cefazolin). Using at
hyperenzymes type in order to prevent septic
complications in bliliary etiology of CP.
Novocain (0,24% solution 150-200 ml) – in order to
analgesia, spasmodics reduced pain.
 Treatment of exocrine pancreatic
insufficiency
Replacement therapy drugs containing predominantly
lipase (10-25 thousand) (Creon 25000, Pangrol,
Mezim Fort. 15000 units lipase).
If is necessary the dose is increased.
Recommended products in capsules, which contain
the mini pill-1,2 mm. in diameter, enteric-coated
shell, which dissolve within 1-2 min.
Liberation of enzymes from the capsule is faster and
more completely at pH-5,5
The above mentioned drugs improve digestion,
reducing steatorheea.
 Prognosis
CP in most causes – a gradual incurable disease
with multiple complications os long term course
of illness.
In the progressive forms of the disease with a
duration of more than 7-10 years, mortality is
high (untreated).
Leading causes of death in the progression of
the disease (untreated) is associated with tumors
and liver diseases.
The stopped using of alcohol and tobacco
increases the duration of the life in patients with
CP.
 Prophylaxis
Primary prevention – removal of risk factors (alcohol,
smoking, obesity, overeating etc.)

Secondary prevention – treatment of relapses, removal

factors what worsening course of disease (treatment of
biliary diseases, obstructions, cysts, tumors), regulation
of fat, carbohydrates changes, level of Ca in blood etc.)

Third prevention – diagnosis of complications and

treatment of theirs