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 pancreatitisInfections:

A. MumpsB. Viral hepatitisC. Echovirus, CoxackievirusD. AscariasisE. Mycoplasma

Penetrating peptic ulcer Obstruction of Ampula of Vater Pancreas divisum Systemic lupus eritematous

Thrombotic thrombocytopenic purpuraNecrotizing 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 peritoneal space

- increase release of kinin peptides which cause vasodilatation andvascular 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 APSonography 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. LOCALA. PA phlegmonB. PA abcessC. Pa pseudocyst

II. SYSTEMICA. Pulmonary:1. pleural effusion2. atelectasis3. mediastinal abcess4. pneumonitis

B. C.V.1. hypotension2. sudden death3. pericardial effusion4. non-specific ST-T changes simulating myocardial infarction.

C. HEMATOLOGIC- DIC

D. GI HEMORRHAGE1. peptic ulcer2. erosive gastritis3. hemorrhage pancreatic necrosis + erosion into major blood vessels4. Portal vein thrombosis, variceal hemorrhageE. RENAL1. oliguria2. azotemia3. renal vein thrombosis

F. METABOLIC1. hyperTG2. glycemia33 Ca, ehp4. Sudden blindness(PURTSCHER retinopathy)G. CENTRAL NERVOUS SYSTEM1. psychosis2. 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 alcoholism2. Cystic fibrosis3. Severe protein caloric malnutrition with hypoalbuminemia4. Pancreatic and duodenal neoplasm5. Pancreatic resection6. Gastric surgery: Billroth II, I anastomoses, truncal vagotomy and pyloroplasty7. Gastrinoma (Zollinger – Ellison syndrome)8. Hereditary pancreatitis9. Traumatic PA10. Hemochromatosis11. Trypsinogen deficiency12. Enterokinase deficiency13. Amylase, lipase or proteases deficiency14. antitrypsin deficiency15. 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:PAINMALABSORBTION

Avoid alcoholStricture 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 pain75% Weight loss Jaundice( head only 80% Courvoisier' s sign

Glucose intolerancePalpable gallbladderMigrathory thrombophlebitisGI hemorrhageSplenomegaly

DIAGNOSTIC PROCEDURES

CEACA19-9CT - retroperitoneal lymph nodes, pelvisUSMRIERCP - 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.

LaparotomySuperficial 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 HEPATITISDEFINITION: 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 vomitingLiver 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 medical centers with therapeutic trials.

- nitrofurantoin

- benzodiasepines

Chemicals , radiations

CLINICAL FEATURES

FatigueJaundiceMalaiseAnorexiaLow Grade FeverAmenorrheaBloody DiarrheaArtralgia / ArthritisPapular EruptionsAcneaErythema NodosumPleuresyPericarditisAnemia

TreatmentPrednison:20-40mg/day,1o-

20mg/day-1year;AZT:50-75mg/day

LABORATORY FINDINGS

BT, AP, glob. TGO, TGPHypoalbuminemiaIP Autoantibodies DNA

Ig 6smooth musclemitochondria

LIPID INFILTRATIONSFATTY 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.

ETIOLOGYCauses depend and the age

geographic location metabolic – nutritional status

Chronic alcoholisation – duration and degree of alcoholic excessProtein mallnutrition in infancy and early childhood in the tropical zones of Africa, South America, AsiaDiabetes mellitusObesityJejun ileal bypass for surgical treatment of morbid obesityProlonged i.v. hyperalimentationAcute 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 intake2. removal of alcohol / correction of metabolic disorders

DIAGNOSIS:

Hepatomegaly nontenderPBH – sometimesLab. findings

REYE’S SYNDROME

(FATTY LIVER WITH ENCEPHALOPATHY)

Children 15 years Cause: unknownClinical: vomiting TGP, TGO viral,

SNC damage > TP toxico-agents +hypoglicemia amonemia salycylatesjaundice- minimal

Major extrahepatic changes: fatty changes of the renal tubular cellscerebral edemaneuronal 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 wall2. chemical inflamation: release of lysolecitin - local factors3. bacterial inflamation: Escherichia coli

Klebsiella speciesStreptococcusStaphylococcus speciesClostridium 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 EXAMINATIONLABORATORY: leukocystosys≥ 10000/ml ↑ BT, TGO, TGPU.S.- stones→ 95% casesTREATMENT: 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 CHOLECYSTITISA. Empyema C. GangreneB. Hydrops D. Perforation

A. Cholangitis: ↑ feversevere right upper quadrant painleukocytoses

Sepsis→ perforationEmergency 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:empyemaperforationGangrene

C. Ischemia of the wall →complete necrosis

D. Localized- abcess formationFree perforation →peritonitis

E. Fistulization into an adiacent organ:duodenum stomachjejunumhepatic flexure of the colonabdominal wall renal pelvis

F. Porcelain GBcalcium salts deposition within the wall of a chronically inflamed GB→ plain abdominal film.

Complication - carcinoma of the GB → cholecystectomy

TREATMENT1. 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 FEATURESright upper quadrant pain weight lossjaundicepalpable mass± cholangitisSPREAD → lymphatic and hematogenous routes

DIAGNOSTICU.S.C.T. R.M.N. Laparotomy

TREATMENTRadical operative resectionRadiation doesn’t appear to improve survival.Chemotherapy