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Table 37-3. Colorectal Cancer (CRC) Screening and Surveillance Recommendations

Indication	Recommendations
Average risk	Any one of the following beginning at age 50:
(سابقه فردی و خانوادگی برای کنسر کولون ندارند)	Annual fecal occult blood testing (FOBT)
	Flexible sigmoidoscopy every 5yr
	Annual FOBT plus flexible sigmoidoscopy every 5yr
	Double-contrast barium enema every 5yr
	Colonoscopy every 10yr
1-2 first-degree relatives with CRC at any age or adenoma(s) at age <60	Same options for average risk beginning at age 40
Hereditary nonpolyposis colorectal cancer = سندرم لینچ در خانواده دارند	Genetic counseling/screening *اسکرین از 25 سالگی با کولونوسکوپی هر 1-2 سال تا 40 سالگی سپس سالی یکبار.
	Colonoscopy every 1-2 years beginning at age 25 and then yearly after age 40†
Familial adenomatous polyposis(FAP)/ Gardner's syndrome	Genetic counseling/testing *شروع از بلوغ با سیگموئیدوسکوپی قابل انعطاف سالیانه+اسکرین برای ژن APC
	Flexible sigmoidoscopy yearly beginning at puberty†
Personal history of CRC (Colorectal Cancer)	Colonoscopy within 1yr of curative resection; repeat at 3yr and then every 5yr if normal
Personal history of colorectal adenoma(s)	Colonoscopy every 3-5yr after removal of all index polyps
Inflammatory bowel disease	Colonoscopy every 1-2yr beginning after 8yr of pancolitis or after 15yr if only left-sided disease در مورد PSC+UC سالی یکبار کولونوسکوپی می کنیم
*Whenever possible, affected relatives should be tested first because of potential false-negative results. †Screening recommendation for individuals with positive or indeterminate tests as well as for those who refuse genetic testing.

Congenital hypertrophy of the retinal pigment epithelium is an early benign manifestation of both FAP and Gardner's syndrome.

سندرم های پارانئوپلاستیک  در آدنوکارسینومای معده:

A variety of paraneoplastic syndromes have been associated with gastric adenocarcinoma and warrant an investigation for a gastrointestinal malignancy. They include:

Trousseau's syndrome (thrombosis),

acanthosis nigricans (pigmented dermal lesions),

membranous nephropathy,

microangiopathic hemolytic anemia,

Leser-Trélat sign (seborrheic keratosis), and

dermatomyositis.

نئوپلاسمهای کبدی:

آدنوم های کبدی

Hepatic Adenomas:

found predominantly in women of childbearing age, are associated with estrogen and oral contraceptive use, and may enlarge during pregnancy. in Men use of anabolic steroids -- usually incidentally identified -- can spontaneously hemorrhage during menstruation or pregnancy or postpartum, causing shock and requiring surgical resection-- Consist of normal hepatocytes without portal tracts and Kupffer cells.

The diagnosis is suggested by the appearance of a cold spot on technetium-99m-sulfur colloid scans (resulting from absence of Kupffer cells) and of vascular lesions on angiography.

The appearance on ultrasonography, computed tomography, and magnetic resonance imaging is nonspecific, but a characteristic feature is the presence of a well-defined capsule.

همانژیوم های کبدی:

Hemangiomas

are the most common mesenchymal hepatic neoplasms -- prevalence in the general population of 2 to 5%-- usually discovered incidentally--most often solitary and located in the right lobe of the liver.

Right upper quadrant abdominal pain may occur in patients with large lesions (typically > 5 cm) owing to the development of intratumoral hemorrhage and thrombosis.

Diagnosisà readily made when a hyperechoic lesion on ultrasound evaluation corresponds to a peripheral enhancing lesion that eventually completely fills during dynamic computed tomography, when MRI reveals a high-intensity signal on T2-weighted images (most sensitive test), or when a technetium-99m red blood cell scan (most specific test) shows retention of the isotope in the tumor.

Treatment is usually not necessary in lesions less than 5 cm. In larger lesions, close monitoring and/or elective resection has been advocated. Symptomatic lesions may be treated with embolization, enucleation, resection, and, in extreme cases, transplantation (large unresectable lesions or multiple lesions).

Table 44-1. Hepatocellular Carcinoma

Incidence

From 1-7 per 100,000 to >100 per 100,000 in high-risk areas

Sex

4:1 to 8:1 male preponderance

Associations

Chronic hepatitis B infection

Chronic hepatitis C infection

Hemochromatosis (with cirrhosis)

Cirrhosis (alcoholic, cryptogenic)

Aflatoxin ingestion

Thorotrast

α1-Antitrypsin deficiency

Androgen administration

Common Clinical Presentations

Abdominal pain

Abdominal mass

Weight loss

Deterioration of liver function

Unusual Manifestations

Bloody ascites

Tumor emboli (lung)

Jaundice

Hepatic or portal vein obstruction

Metabolic effects

Erythrocytosis

Hypercalcemia

Hypercholesterolemia

Hypoglycemia

Gynecomastia

Feminization

Acquired porphyria

Clinical/Laboratory Findings

Hepatic bruit or friction rub

Serum α-fetoprotein level >400 ng/mL

Indeed, in 10 to 20% of patients, no cause for granulomas is found despite extensive investigation. A subset of these patients have a syndrome consisting of fever, hepatomegaly, and hepatic granulomas that responds to corticosteroids, described as hepatic granulomatous disease or "granulomatous hepatitis." These patients may possibly have a variant of sarcoidosis.

Liver biopsy (and culture, particularly for acid-fast bacteria) is of considerable value in the diagnosis of sarcoidosis, miliary tuberculosis, and disseminated histoplasmosis, because virtually all patients with these disorders have hepatic granulomas.

Characteristic granulomas are seen in many patients with primary biliary cirrhosis, and granulomas may be the first clue to Hodgkin's disease.

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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.

Table 45-1. Risk Factors for Cholelithiasis

Primary

Age

Obesity

Female sex

Rapid weight loss

Race (e.g., Native American)

Secondary

Use of oral contraceptives

Pregnancy

Diabetes mellitus

Use of insulin

Low socioeconomic status

Sedentary lifestyle

Total parenteral nutrition

Hemolysis

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,

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.

Table 38-1. Etiology of Acute Pancreatitis

Obstructive Causes

Gallstones

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

Toxins

Ethyl alcohol

Methyl alcohol

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

Organophosphorus insecticides

Drugs

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

Trauma

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

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

Infectious

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

Vascular

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

Vasculitis-systemic lupus erythematosus, polyarteritis nodosa, malignant hypertension

Idiopathic

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

Miscellaneous

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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