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 pancreatitits
I nfections:
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 retroperitoneal space
- increase release of kinin peptides which cause vasodilatation
andlvascular permeability
- systemic effects of protheolytic + lypolytic enzymes released into
the
Jaundice! circulation.
Erythematous skin nodules (s.c. fat necrosis)
Basilar rals, atelectasis, pleural effusion (left-sided)
Abdominal tenderness, muscle rigidity
Bowel sounds are diminished or absent
Pancreatic pseudocyst palpable in the upper abdomen
Faint blue discoloration around the umbilicus- Cullens sign result of
hemoperitoneum.
Blue-red-purple/ green brown coloration of the flanks Turners sign tissue
catabolism of Hb.
LABORATORY DATA

increase serum amylase. After 48-72h return to normal with treatment.
leukocytosis: 15-20000/mm
3

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

E. RENAL
1. oliguria
2. azotemia
3. renal vein thrombosis

F. METABOLIC
1. hyperTG
2. l glycemia
3. Ca, Encephalopathy,sudden blindness-Purtscher s retinopathy-

G. CENTRAL NERVOUS SYSTEM
1. psychosis
2. fat emboli


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.

TREATMENT
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. o 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 radiating to the back
(continous / intermittent / absent)

deep
neresponsive to antiacids
increased by alcohol and heavy meals

2. Weight loss

3. Abnormal stools
DIAGNOSIS EVALUATION

Colestasis:
| FA
| amylase = lipase levels
| bilirubine
Steatorrhea
Diabetes mellitus CP and exocrine PA insufficiency
B12 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 head 70%
Alcohol body 20%
Cronic Pa tail 10%
Cholelitiasis

CLINICAL FEATURES:

Abdominal pain
75% 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 encacasement of
peripancreatic vessels is present importance in determining te
potential for surgical resection.

Laparotomy
Superficial biopsy may not show neoplastic tissue since the
cancer itself is often surrounded by endematous, inflamed, fibrotic
tissue.
TREATMENT

Complete surgical resection of PA tumors offers the only
effective treatement 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 symphtoma
poliart.
Chemoteraphy 5FU + irradiation
CHRONIC HEPATITIS

CHRONIC PERSISTENT HEPATITIS
DEFINITION: result from infection with HVB, HCV hepatitis viruses.
AgHBs + CrAHD

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- Zeffix ( Lamivudin 100mg/day - 2years ITF)
AcAHVC Interferon (Pegintron /Pegasis+ Ribavirin)
Drugs:
- methyldopa
- isoniazid medical centers with therapeutic trials.
- nitrofurantoin
- benzodiasepines
Chemicals , radiations
CLINICAL FEATURES

Fatigue
Jaundice
Malaise
Anorexia
Low Grade Fever
Amenorrhea
Bloody Diarrhea
Artralgia / Arthritis
Papular Eruptions
Acnea
Erythema Nodosum
Pleuresy
Pericarditis
Anemia
Treatment:PDN:20-
40mg/day-10-
20mg/day1year+AZT50-
75mg
LABORATORY FINDINGS

| BT, PA, 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 is 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 - 12g 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
REYES SYNDROME

(FATTY LIVER WITH ENCEPHALOPATHY)

Children < 15 years Cause: unknown
Clinical: vomiting | TGP, TGO viral,
SNC damage | TP toxico-agents +
hypoglicemia |amonemia salycylates
jaundice minimal

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
GAUCHERS DISEASE

deficiency of the enzyme glucosylceramide - | glucosidaze in
pheripheral leucocytes
acumulation of large RE cells containing the cerebroside
glucosylceramide (Gauchers cells) in the liver, spleen
- hepatosplenomegaly
- ascites
- HTP compression of the intrahepatic vasculation
WILSONS 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)
LIVER TRANSPLANT
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 - Murphys 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>
cases.
- may be asymptomatic for years GBD
acute cholecystitis
COMPLICATIONS OF CHOLECYSTITIS
A. Empyema C. Gangrene
B. Hydrops D. Perforation

A. Cholangitis: 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 in 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 doesnt appear to improve survival.
Chemotherapy