definition: pancreatic inflamatory disease. clasification: edematous pancreatitis – mild and self...
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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
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