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سه‌شنبه 6 شهریور‌ماه سال 1386
ادامه گوارش + پانکراس



Ammonia, derived from both amino acid deamination and bacterial hydrolysis of nitrogenous compounds in the gut, has been implicated in the pathogenesis of hepatic encephalopathy, but its blood levels correlate poorly with the presence or degree of encephalopathy.


A number of potential contributors to hepatic encephalopathy have been investigated. These include γ-aminobutyric acid, mercaptans, short-chain fatty acids, benzodiazepine-like compounds, imbalance between plasma branched-chain and aromatic amino acids, altered cerebral metabolism (disturbed Na+, K+-ATPase activity), zinc deficiency, and deposition of manganese in the basal ganglia.


Protein restriction may be considered in patients with severe encephalopathy, but long-term restriction is associated with worsening malnutrition.

 Nonabsorbable disaccharides (i.e., lactulose) are fermented to organic acids by colonic bacteria, lowering stool pH and trapping ammonia in the colon, and thereby preventing diffusion.

Reduction and elimination of nitrogenous compound substrates can be achieved by administration of enemas and the use of antibiotics that reduce colonic bacteria (i.e., neomycin and metronidazole).

Treatment with formulas rich in branched-chain amino acids has shown no benefit in improving encephalopathy or mortality.



The pathophysiology of this syndrome involves intrapulmonary vascular dilation in the absence of architectural damage.

The vascular dilation leads to impaired oxygen transfer from alveoli to the central stream of red blood cells within capillaries, with a resulting "functional" intrapulmonary right-to-left shunt that improves with 100% oxygen!!!!

Intrapulmonary vascular dilation is detected by contrast echocardiography, which shows delayed visualization of microbubbles in the left heart chambers.

Table 45-1. Risk Factors for Cholelithiasis





Female sex

Rapid weight loss

Race (e.g., Native American)


Use of oral contraceptives


Diabetes mellitus

Use of insulin

Low socioeconomic status

Sedentary lifestyle

Total parenteral nutrition


Biliary parasites (e.g., Clonorchis sinensis)

The pathophysiology of pigment stones is less well understood; however, increased production of bilirubin conjugates (hemolytic states), increased biliary Ca2+ and HCO3-, cirrhosis, and bacterial deconjugation of bilirubin to a less soluble form are all associated with pigment stone formation.

  1. Biliary cholesterol saturation is increased by estrogens, multiparity, oral contraceptives, obesity, rapid weight loss, and terminal ileal disease (which decreases the bile acid pool).
  2. Nucleation is enhanced by biliary parasites, recurrent bacterial infection of the biliary tract, and antibiotics such as ceftriaxone (which has a proclivity to concentrate and crystallize with calcium in the biliary tree). Total parenteral nutrition and blood transfusions also promote bile pigment accumulation and "gelfaction" of sludge.
  3. Bile stasis is caused by gallbladder hypomotility (resulting from pregnancy, somatostatin, or fasting), bile duct strictures, choledochal cysts, biliary parasites, and total parenteral nutrition

کوله سیستکتومی پروفیلاکتیک:

Asymptomatic patients should be followed expectantly. Prophylactic cholecystectomy is considered in groups at increased risk for developing complications:

(1) diabetics who have a greater morbidity and mortality from acute cholecystitis;

(2) persons with a calcified (porcelain) gallbladder or large gallbladder polyps, which are associated with an increased risk of carcinoma of the gallbladder;

(3) persons with sickle cell anemia, in whom hepatic crises may be difficult to differentiate from acute cholecystitis; and

(4) children with gallstones, because they frequently develop symptomatic disease.


Mirizzi syndrome is the occurrence of profound jaundice resulting from extrinsic compression of the common hepatic duct by an impacted stone in the cystic duct at the gallbladder neck.


BILIARY NEOPLASMS: Risk factors for development of these cancers include:

primary sclerosing cholangitis,

chronic ulcerative colitis,

choledochal cysts,


C. sinensis,

hepatolithiasis, and

α1-antitrypsin deficiency.




Elevated serum pancreatic enzymes may occur in a variety of other conditions, including bowel perforation, intestinal obstruction, mesenteric ischemia, tubo-ovarian disease, and renal failure. Serum lipase is slightly more specific and remains normal in some conditions associated with an elevation of serum amylase, including macroamylasemia, parotitis, and tubo-ovarian disease.




Table 38-1. Etiology of Acute Pancreatitis


Obstructive Causes


Tumors-ampullary or pancreatic tumors

Parasites-Ascaris or Clonorchis

Developmental anomalies-pancreas divisum, choledochocele, annular pancreas

Periampullary duodenal diverticula

Hypertensive sphincter of Oddi

Afferent duodenal loop obstruction


Ethyl alcohol

Methyl alcohol

Scorpion venom-excessive cholinergic stimulation causes salivation, sweating, dyspnea, and cardiac arrhythmias; seen mostly in the West Indies

Organophosphorus insecticides


Definite association (documented with rechallenges): azathioprine/6-MP, valproic acid, estrogens, tetracycline, metronidazole, nitrofurantoin, pentamidine, furosemide, sulfonamides, methyldopa, cytarabine, cimetidine, ranitidine, sulindac, dideoxycytidine

Probable association: thiazides, ethacrynic acid, phenformin, procainamide, chlorthalidone, l-asparaginase

Metabolic Causes

Hypertriglyceridemia, hypercalcemia, end-stage renal disease


Accidental-blunt trauma to the abdomen (car accident, bicycle)

Iatrogenic-postoperative, ERCP, endoscopic sphincterotomy, sphincter of Oddi manometry


Parasitic-ascariasis, clonorchiasis

Viral-mumps, rubella, hepatits A, hepatitis B, non-A, non-B hepatitis, coxsackievirus B, echo, adenovirus, cytomegalovirus, varicella, Epstein-Barr, human immunodeficiency virus

Bacterial-mycoplasma, Campylobacter jejuni, tuberculosis, Legionella, leptospirosis


Ischemia-hypoperfusion (such as after cardiac surgery) or atherosclerotic emboli

Vasculitis-systemic lupus erythematosus, polyarteritis nodosa, malignant hypertension


10-30% of pancreatitis; up to 60% of these patients have occult gallstone disease (biliary microlithiasis or gallbladder sludge); other less common causes include sphincter of Oddi dysfunction and mutations in the cystic fibrosis transmembrane regulator


Penetrating peptic ulcer

Crohn's disease of the duodenum

Pregnancy associated

Pediatric association-Reye's syndrome, cystic fibrosis




Table 38-2. Signs Used to Assess Severity of Acute Pancreatitis


At Time of Admission or Diagnosis

Age >55 yr

White blood cell count >16,000/mm3

Blood glucose >200 mg/dL

LDH >2 × normal

ALT >6 × normal

During Initial 48 hr

Decrease in hematocrit >10%

Serum calcium <8 mg/dL

Increase in blood urea nitrogen >5 mg/dL

Arterial PO2 <60 mmHg

Base deficit >4 mEq/L

Estimated fluid sequestration >6000 mL

Mortality is approximately 1% when there are fewer than three Ranson's signs, 10 to 20% when there are three to five signs, and greater than 50% when there are six or more Ranson's signs.


For removal of impacted gallstones or establishment of biliary drainage indicated for patients with evidence of biliary sepsisàEmergency ERCP à followed by elective cholecystectomy.


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