ادامه گوارش + پانکراس
HEPATIC ENCEPHALOPATHYانسفالوپاتی کبدی
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.
Treatment:
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.
HEPATOPULMONARY SYNDROMEسندرم هپاتوپولموناری
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.
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Table 45-1. Risk Factors for Cholelithiasis |
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.
- Biliary cholesterol saturation is increased by estrogens, multiparity, oral contraceptives, obesity, rapid weight loss, and terminal ileal disease (which decreases the bile acid pool).
- 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.
- 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,
gallstones,
C. sinensis,
hepatolithiasis, and
α1-antitrypsin deficiency.
پانکراس:
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.
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Table 38-1. Etiology of Acute Pancreatitis |
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Table 38-2. Signs Used to Assess Severity of Acute Pancreatitis |
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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