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ACUTE

ACUTE. PANCREATITIS. DEFINITION: pancreatic inflamatory disease. CLASIFICATION: edematous pancreatitis – mild and self – limited disease; necroziting pancreatitis – severity of the attack and its systemic manifestation;

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ACUTE

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  1. ACUTE PANCREATITIS

  2. 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.

  3. 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

  4. 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.

  5. 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.

  6. 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 andvascularpermeability • - 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.

  7. 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

  8. DIAGNOSIS: anamnesis, clinical features, laboratory studies. • DIFFERENTIAL DIAGNOSIS: • Perforated viscers – peptic ulcer • Acute cholecystitis and biliary colic • Acute intestinal obstruction • Mesenteric vascular occlusion • Renal colic • Myocardial infarction • Dissecting Ao anevrysm • Pneumonia • Diabetic ketoacidosis • Vasculitis

  9. COMPLICATIONS • I. LOCAL • A. PA phlegmon • B. PA abcess • C. Pa pseudocyst • II. SYSTEMIC • A. Pulmonary: • pleural effusion • atelectasis • mediastinal abcess • pneumonitis • B. C.V. • hypotension • sudden death • pericardial effusion • non-specific ST-T changes simulating myocardial infarction.

  10. C.HEMATOLOGIC • - DIC • D. GI HEMORRHAGE • peptic ulcer • erosive gastritis • hemorrhage pancreatic necrosis + erosion into major blood vessels • 4. Portal vein thrombosis, variceal hemorrhage • E. RENAL • oliguria • azotemia • renal vein thrombosis • F. METABOLIC • hyperTG •  glycemia •  Ca, ehp • 4. Sudden blindness(PURTSCHER retinopathy) • G. CENTRAL NERVOUS SYSTEM • psychosis • fat emboli

  11. Medical therapy - reducing PA secretion “putting the PA on rest” • analgesis for pain - i.v. fluids and colloids- maintain normal intravascular volume • no oral alimentation • nasogastric suction • antibiotic therapy • parenteral nutrition • laparatomy with adecquate drainage and removal of necrotic tissue. TREATMENT

  12. 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 • 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.

  13. 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 • 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

  14. 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

  15. 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

  16. 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

  17. 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.

  18. 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

  19. 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.

  20. CHRONIC ACTIVE HEPATITIS • hepatic necrosis • active inflamatory ± lead  liver failure, cirrhossis, death. • fibrosis • AUTOIMUNE • LUPOID • CHRONIC ACTIVE LIVER DISEASE

  21. 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

  22. ETIOLOGY • Alcohol • AgHBs • AgHVC • Drugs: • - methyldopa • - isoniazid medical centers with therapeutic trials. • - nitrofurantoin • - benzodiasepines • Chemicals , radiations

  23. 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,1o-20mg/day-1year;AZT:50-75mg/day LABORATORY FINDINGS BT, AP,  glob.  TGO, TGP Hypoalbuminemia IP  Autoantibodies DNA Ig 6 smooth muscle mitochondria

  24. 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

  25. 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

  26. REYE’S 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

  27. 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

  28. 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

  29. 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.

  30. 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.

  31. 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

  32. 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

  33. 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

  34. 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

  35. 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.

  36. POSTCHOLECYSTECTOMY SYNDROME SYMPTOMS of : reflux esophagitis peptic ulceration pancreatitis IBS SYNDROMESdue to: biliary strictures retained biliary calculi cystic duct strump syndrome stenosis or dyskinesia of the sphincter Oddi bile salt - induced diarrhea / gastritis.

  37. 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 doesn’t appear to improve survival. Chemotherapy

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