DEFINITION: pancreatic inflamatory disease.
CLASIFICATION:
 edematous pancreatitis – mild and self – limited disease;
 necroziting pancreatitis – severity of the attack and its systemic
manifestation;
 hemorrhagic pancreatitis – also in: - pancreatic trauma;
- pancreatic carcinoma;
- congestive heart failure.
ETIOLOGIC FACTORS AND PATHOGENESIS
 Alcohol
 Gallstones
 Metabolic factors (  TGO,  Ca, hyperparathyroidism, renal failure, acute
fatty liver of pregnancy, after renal transplant)
 Drugs (Azathioprine, Thiazide diuretics, Estrogens, Tetracycline, Sulfonamides)
 Postoperator (abdominal, nonabdominal)
 Postendoscopic retrograde cholangiopancretography (ERCP)
 Trauma
 Hereditary pancreatitis
Infections:
A. Mumps
B. Viral hepatitis
C. Echovirus, Coxackievirus
D. Ascariasis
E. Mycoplasma
 Penetrating peptic ulcer
 Obstruction of Ampula of Vater
 Pancreas divisum
 Systemic lupus eritematous
Thrombotic thrombocytopenic purpura
Necrotizing angitis
PATHOGENIC THEORIES
1.
Autodigestion
by
proteolytic
enzymes
trypsinogen,
chymotripsinogen, proelastase, phospholipase A are activated within
the pancreas rather than in the intestinal lumen.
The active enzymes digest then the cellular membranes
- cause protheolysis, edema, interstitial hemorrhage
- cellular injury and death result from eliberation of activated
enzymes.
Activation of bradykinin peptides and histamine produce
vasodilatation, increase vascular permeability, edema.
 Cascade of events culminating in the development of ACUTE
NECROTIZING PANCREATITIS.
2. Reflux of bile into the pancreatic duct  activation of pancreatic
enzymes.
3. Obstruction + hypersecretion. Lysosomal hydrolases within the
pancreas acinar cell itself.
CLINICAL FEATURES
1. Abdominal pain – steady and boring.
- epigastrium region + periombilical which radiates to the back, chest,
flanks, lower abdomen.
- more intense in supine.
- Relief: by sitting with the trunk flexed and drawn up.
2. Nausea, vomiting, abdominal distension  intestinal hypomotility and
chemical peritonitis.
PHYSICAL EXAMINATION
 Anxious patient
 Low- grade fever
 Tachycardia
 Hypotension
 Shock results from:
- hypovolemia secondary to exudation of blood or plasma proteins
into the
andvascular
peritoneal space
- increase release of kinin peptides which cause vasodilatation
permeability
- systemic effects of protheolytic + lypolytic enzymes released into
the
circulation.
 Erythematous skin nodules
 Basilar rals, atelectasis, pleural effusion
 Abdominal tenderness, muscle rigidity
 Bowel sounds are diminished or absents
 Pancreatic pseudocyst palpable in the upper abdomen
 Faint blue discoloration around the umbilicus- Cullen´s sign result of
hemoperitoneum.
 Blue-red-purple/ green brown coloration of the flanks Turner´s sign tissue
catabolism of Hb.
LABORATORY DATA
 increase serum,urinary amylase,lipase. After 48-72h return to normal
with treatment.
 leukocytosis: 15-20000/mm3
 hyperglicemia
 hypocalcemia 25%
 hypertrigliceridemia 20%
 hyperbilirubinemia10%
 hypoxemia (p O2 ≤ 60 mm Hg)
 ST segment + T wave abnormal  myocardial ischemia.
Rx studies chest, kidney, bladder for excluding other causes.
CT- severity of AP
Sonography
evaluation of gallbladder and biliary tree.
Radionuclid scaning
DIAGNOSIS: anamnesis, clinical features, laboratory studies.
DIFFERENTIAL DIAGNOSIS:
1. Perforated viscers – peptic ulcer
2. Acute cholecystitis and biliary colic
3. Acute intestinal obstruction
4. Mesenteric vascular occlusion
5. Renal colic
6. Myocardial infarction
7. Dissecting Ao anevrysm
8. Pneumonia
9. Diabetic ketoacidosis
10. Vasculitis
COMPLICATIONS
I. LOCAL
A. PA phlegmon
B. PA abcess
C. Pa pseudocyst
II. SYSTEMIC
A. Pulmonary:
1. pleural effusion
2. atelectasis
3. mediastinal abcess
4. pneumonitis
B. C.V.
1. hypotension
2. sudden death
3. pericardial effusion
4. non-specific ST-T changes simulating myocardial infarction.
C. HEMATOLOGIC
- DIC
D. GI HEMORRHAGE
1. peptic ulcer
2. erosive gastritis
3. hemorrhage pancreatic necrosis + erosion into major blood vessels
4. Portal vein thrombosis, variceal hemorrhage
E. RENAL
1. oliguria
2. azotemia
3. renal vein thrombosis
F. METABOLIC
1. hyperTG
2.  glycemia
3.  Ca, ehp
4. Sudden blindness(PURTSCHER retinopathy)
G. CENTRAL NERVOUS SYSTEM
1. psychosis
2. fat emboli
TREATMENT
Medical therapy - reducing PA secretion “putting the PA on rest”
1. analgesis for pain - i.v. fluids and colloids- maintain normal
intravascular volume
2. no oral alimentation
3. nasogastric suction
4. antibiotic therapy
5. parenteral nutrition
6. laparatomy with adecquate drainage and removal of necrotic tissue.
CHRONIC PANCREATITIS
DEFINITION: chronic damage with persistent pain or malabsorbtion
( steatorrhea)
CAUSES:
1. Chronic alcoholism
2. Cystic fibrosis
3. Severe protein caloric malnutrition with hypoalbuminemia
4. Pancreatic and duodenal neoplasm
5. Pancreatic resection
6. Gastric surgery: Billroth II, I anastomoses, truncal vagotomy and
pyloroplasty
7. Gastrinoma (Zollinger – Ellison syndrome)
8. Hereditary pancreatitis
9. Traumatic PA
10. Hemochromatosis
11. Trypsinogen deficiency
12. Enterokinase deficiency
13. Amylase, lipase or proteases deficiency
14.  antitrypsin deficiency
15. Idiopatic PA.
PATHOPHYSIOLOGY
- Precipitation of protein within the ducts
Ductal obstruction  duct dilatation, diffuse atrophy of the acinar cells,
fibrosis, calcifications of the protein plugs.
CLINICAL FEATURES
1. Pain
in
epigastric
region
(continous / intermittent / absent)
– deep
– neresponsive to antiacids
– increased by alcohol and heavy meals
2. Weight loss
3. Abnormal stools
radiating
to
the
back
DIAGNOSIS EVALUATION
Colestasis:
 FA
 amylase = lipase levels
 bilirubine
Steatorrhea
Diabetes mellitus
B12
 CP and exocrine PA insufficiency
malabsorbtion
Radiographic hallmark: scattered calcification through the pancreas.
Ultrasound: pseudocysts
CT - calcifications, pseudocysts.
ERCP- direct view of the pancreatic duct
COMPLICATIONS
 DM
 Effusions within the pleura, pericardium, peritoneum.
 GI bleeding: peptic ulcer, gastritis, pseudocysts eroding in duodenum.
 Icterus- cholangitis, biliary cirrhosis.
 Subcutaneous fat necrosis.
TREATMENT
Therapy is directed  2 major problems:
PAIN
MALABSORBTION
Avoid alcohol
Stricture in the PA duct  local resection may ameliorate pain.
PA enzyme replacement therapy.
Hereditary PA - rare form of PA:
- PA calcifications
- D.M.
- Steatorrhea
- PA carcinoma
PANCREATIC CANCER
Males, blacks  50 years.
Risk factors:
Smoking
Alcohol
Cronic Pa
Cholelitiasis
head 70%
body 20%
tail 10%
CLINICAL FEATURES:
75%
Abdominal pain
Weight loss
Jaundice( head only 80%  Courvoisier' s sign
Glucose intolerance
Palpable gallbladder
Migrathory thrombophlebitis
GI hemorrhage
Splenomegaly
DIAGNOSTIC PROCEDURES
CEA
CA19-9
CT - retroperitoneal lymph nodes, pelvis
US
MRI
ERCP - stenosis/ obstruction of the pancreatic selective and
superselective angiography CBP
body + tail CA  vascular narrowing displacement
occlusion / by tumor
Angiography is useful in assessing whether encasement of
peripancreatic vessels is present  importance in determining the
potential for surgical resection.
Laparotomy
Superficial biopsy may not show neoplastic tissue since the
cancer itself is often surrounded by edematous, inflamed, fibrotic
tissue.
TREATMENT
Complete surgical resection of PA tumors offers the only
effective treatment for this disease.
The median survival for patients whose PA cancers are
surgically unresectable is aprox 5 months.
BDA  surgical diversion of the biliary system –
symphtomatic palliation.
Chemoteraphy 5FU + irradiation
CHRONIC HEPATITIS
CHRONIC PERSISTENT HEPATITIS
DEFINITION: result from infection with HVB, HCV hepatitis viruses.
AgHBs + AHVD.
PATHOLOGY: infiltration of the portal areas with MN cells no erosion of the
limiting plate or extension of the inflammation into the liver lobule.
CLINICAL& LABORATORY FEATURES:
• fatigue
• anorexia
• nausea and vomiting
Liver slightly enlarged and tender.
Mild elevation of aminotransferase +FA months years.
No specific theraphy !
Follow-up examination every 6-12 months, until ..... have return to normal and
to identify patients who may progress to chronic active hepatitis.
CHRONIC ACTIVE HEPATITIS
 hepatic necrosis
 active inflamatory ± lead  liver failure, cirrhossis, death.
 fibrosis
AUTOIMUNE
LUPOID
CHRONIC ACTIVE LIVER DISEASE
PATHOLOGY
Liver biopsy is necessary to establish the diagnosis.
The cardinal histopathologic features include:
 a dense mononuclear + plasma cell infiltraton of the portal zones which
expands into the liver lobule.
 destruction of the hepatocytes at the periphery of the lobule( piecemeal
necrosis).
 connective tisssue septa extending from the portal zones into the lobule,
isolating parenchymal cells into clusters and enveloping bile ducts.
 regenerative ,,pseudolobules”
 multilobular bridging hepatic necrosis
ETIOLOGY
 Alcohol
 AgHBs
 AgHVC
 Drugs:
- methyldopa
- isoniazid
- nitrofurantoin
- benzodiasepines
 Chemicals , radiations
medical centers with therapeutic trials.
CLINICAL FEATURES
Fatigue
Jaundice
Malaise
Anorexia
Low Grade Fever
Amenorrhea
Bloody Diarrhea
Artralgia / Arthritis
Papular Eruptions
Acnea
Erythema Nodosum
Pleuresy
Pericarditis
Anemia
Treatment
Prednison:20-40mg/day,1o20mg/day-1year;AZT:5075mg/day
LABORATORY FINDINGS
 BT, AP,  glob.
 TGO, TGP
Hypoalbuminemia
IP 
Autoantibodies
DNA
Ig 6
smooth muscle
mitochondria
LIPID INFILTRATIONS
FATTY LIVER
Although minimal fatty changes are often transient and have no
clinical significance, persistent / extensive fatty infiltration may produce
dysfunction + symptoms that require careful evaluation.
ETIOLOGY
Causes depend and the  age
 geographic location
 metabolic – nutritional status
Chronic alcoholisation – duration and degree of alcoholic excess
Protein mallnutrition in infancy and early childhood in the tropical zones of
Africa, South America, Asia
Diabetes mellitus
Obesity
Jejun ileal bypass for surgical treatment of morbid obesity
Prolonged i.v. hyperalimentation
Acute fatty liver  carbon tetrachloride intoxication
 DDT poisoning
 ingestion of yellow phosphorus
of pregnancy – fatal condition third trimester
Massive tetracycline theraphy 3 ÷ 12 g i.v.
rare cause
CLINICAL FEATURES:
Tenderness over the enlarged liver
 FA, transaminases
TREATMENT
1. adequate nutritional intake
2. removal of alcohol / correction of metabolic disorders
DIAGNOSIS:
Hepatomegaly nontender
PBH – sometimes
Lab. findings
REYE’S SYNDROME
(FATTY LIVER WITH ENCEPHALOPATHY)
Children  15 years
Clinical: vomiting
 TGP, TGO
SNC damage > TP
hypoglicemia
amonemia
jaundice- minimal
Cause: unknown
viral,
toxico-agents +
salycylates
Major extrahepatic changes:
fatty changes of the renal tubular cells
cerebral edema
neuronal degeneration of the brain
Mortality: 50 %
Treatment: infusions of glucose, fresh frozen plasma i.v. mannitol
NIEMANN PICK DISEASE
mainly in Jewish infants
acumulation of sphingomyelin and cholesterol in RE cells of the liver,
spleen, bone marrow, brain, due to deficiency of splingomyelinase
Hepatosplenomegaly
aminotransferase, FA
Diagnostic: bone marrow aspiration – lipid analysis
GAUCHER’S DISEASE
• deficiency of the enzyme glucosylceramide -  glucosidaze in
pheripheral leucocytes
• acumulation
of
large
RE
cells
containing
the
cerebroside
glucosylceramide (Gaucher’s cells) in the liver, spleen 
- hepatosplenomegaly
- ascites
- HTP
compression of the intrahepatic vasculation
WILSON’S DISEASE
young people (pigmentation of the cornea Kayser-Fleischer ring)
• increased copper deposition in the timus
Liver cells are balloned with increase glycogen in the nuclei.
Evolution – cirrhosis (periportal or macronodular)
HEMOCHROMATOSIS
• accumulation of increase iron due to inappropriate absorption in the
intestine
• excess iron in hepatocytes  hepatomegaly
Untreated, progressive impairment is followed by the development of
cirrhosis.
ACUTE COLECYSTITIS
Definition: acute inflamation of the gallbladder (GB) wall follows
destruction of the cystic duct by a stone.
Response is evoked by three factors:
1. mechanical inflamation: increase pressure, distension  ischemic GB
mucosa and wall
2. chemical inflamation: release of lysolecitin - local factors
3. bacterial inflamation: Escherichia coli
Klebsiella species
Streptococcus
Staphylococcus species
Clostridium species
CLINICAL FEATURES
 biliary colic – pain radiates to IS area, right scapula, shoulder
 nausea, vomiting
 fever
 jaundice – involved of bile ducts.
Aprox. 25% palpable GB - Murphy’s sign.
DIAGNOSTIC: HYSTORY+PHYSICAL EXAMINATION
LABORATORY: leukocystosys≥ 10000/ml
↑ BT, TGO, TGP
U.S.- stones→ 95% cases
TREATMENT: USUALLY → surgical intervention.
ALITHIASIC CHOLANGITIS
 Trauma
 Burns
 Postpartum
 Orthopedic/ nonbiliary major surgical operatories
 Vasculitis
 Obstructing adenocarcinoma of the GB
 D.M.
 Torsion of GB
 Bacterial infections: Streptococcus, Leptospira, Salmonella, Vb. Cholerae
 Sarcoidosis
 CV disease
 TBC
 Syphilis
 Actinomycosis
DIAGNOSIS
 US
 CT scanning
 Rx. examination→ large, tense, static GB without stones.
TREATMENT
 AB
 Surgical intervention
CHRONIC CHOLECYSTITIS
Chronic inflammation of GB wall associated with gallstones result from
repeated bouts of acute or subacute cholecystitis bacteria in the bile>
¼ cases.
- may be asymptomatic for years → GBD
→ acute cholecystitis
COMPLICATIONS OF CHOLECYSTITIS
A. Empyema
B. Hydrops
A. Cholangitis:
C. Gangrene
D. Perforation
↑ fever
severe right upper quadrant pain
leukocytoses
Sepsis→ perforation
Emergency surgical intervention with proper antibiotic coverage is required as
soon as the diagnosis is suspected.
B. Result also from prolonged obstruction of the cystic duct, usually by a large
solitary calculus.
Physical examination: - visible easily palpable, nontender mass extending
from the right upper quadrant into the right iliac fossa.
Cholecystectomy – indicated of the potential complications:
empyema
perforation
Gangrene
C. Ischemia of the wall →complete necrosis
D. Localized- abcess formation
Free perforation →peritonitis
E. Fistulization into an adiacent organ:
duodenum
stomach
jejunum
hepatic flexure of the colon
abdominal wall
renal pelvis
F. Porcelain GB
calcium salts deposition within the wall of a chronically inflamed GB→
plain abdominal film.
Complication - carcinoma of the GB → cholecystectomy
TREATMENT
1. Medical therapy:
oral intake eliminated
nasogastric suction
i.v. antibiotic:
ampiciline
cephalosporins
aminoglycosides or combination
chloramphenicol
2. Surgical therapy
Early colecystectomy is the treatment of choice most patients with acute
cholecystitis.
POSTCHOLECYSTECTOMY SYNDROME
SYMPTOMS of :
reflux esophagitis
peptic ulceration
pancreatitis
IBS
SYNDROMES due to:
biliary strictures
retained biliary calculi
cystic duct strump syndrome
stenosis or dyskinesia of the sphincter Oddi
bile salt - induced diarrhea / gastritis.
GALLBLADDER CANCER
Most cancer develop in conjunction with stones rather than polyps.
F / M ratio 4:1 mean age 70 years
CLINICAL FEATURES
right upper quadrant pain
weight loss
jaundice
palpable mass
± cholangitis
SPREAD → lymphatic and hematogenous routes
DIAGNOSTIC
U.S.
C.T.
R.M.N.
Laparotomy
TREATMENT
Radical operative resection
Radiation
Chemotherapy
doesn’t appear to improve survival.