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A GU that fails to heal after 12 weeks and a DU that does not heal after 8 weeks of therapy should be considered refractory.

Alarm features include weight loss, vomiting, dysphagia, evidence of anemia, gastrointestinal bleeding, or an abdominal mass or l

زولینگر-الیسون:

The most common causes of hypergastrinemia are:

antrum-dominant H. pylori infection or

achlorhydria related to either decreased intraluminal acid in the setting of atrophic gastritis or antisecretory therapy with PPIs.

Hypergastrinemia may be related to other causes, including:

retained gastric antrum (after ulcer surgery),

massive small bowel resection,

chronic gastric outlet obstruction, and

chronic renal failure.

Therefore, acid hypersecretion, as documented by gastric acid analysis, is necessary for the diagnosis of ZES.

The diagnosis of ZES is made when there is a fasting gastrin >1000 pg/mL in the setting of gastric acid hypersecretion.

In equivocal cases (e.g., gastrin < 1000 pg/mL),à a positive secretin provocative test will confirm the diagnosis.

The secretin test is positive (≥200 pg/mL increase over the preinjection fasting gastrin level) in approximately 90% of patients with ZES and moderately elevated gastrin levels. Basal acid output is elevated (>15 mmol/hr without previous gastric acid-reducing surgery and >5 mmol/hr with prior surgery) in more than 90% of patients with ZES.

The single best imaging test for gastrinoma is somatostatin receptor scintigraphy (SRS), which is more sensitive than any conventional imaging study.

بیماریهای التهابی روده:

Table 36-2. Differentiating Features

	Ulcerative Colitis	Crohn's Disease
Site of involvement	Only involves colon	Any area of the gastrointestinal tract
	Rectum always involved	Rectal sparing
Pattern of involvement	Continuous	Skip lesions
Diarrhea	Bloody	Usually nonbloody
Severe abdominal pain	Rare	Frequent
Perianal disease	No	In 30% of patients
Fistula	No	Yes
Endoscopic findings	Erythematous and friable	Aphthoid and deep ulcers
	Superficial ulceration	Cobblestoning
Radiologic findings	Tubular appearance resulting from loss of haustral folds	String sign of terminal ileum RLQ mass, fistulas, abscesses
Histologic features	Mucosa only	Transmural
	Crypt abscesses	Crypt abscesses, granulomas (~30%)
Smoking	Protective	Worsens course
Serology	pANCA more common	ASCA more common

ASCA = anti-Saccharomyces cerevisiae antibodies; pANCA = perinuclear antineutrophil cytoplasmic antibodies; RLQ = right lower quadrant.

Table 36-3. Treatment Options

Disease Severity	Ulcerative Colitis	Crohn's Disease
Mild	Oral and topical	5-ASA compounds
	5-ASA compounds	Antibiotics Elemental diet
Moderate	Oral and topical	5-ASA compounds
	5-ASA compounds	Antibiotics
	Oral steroids Azathioprine, 6-MP	Budesonide or oral steroids Azathioprine, 6-MP Methotrexate Infliximab
Severe	IV steroids	IV steroids
	Cyclosporine	Infliximab
	Azathioprine, 6-MP	Azathioprine, 6-MP
	Surgery	Surgery

هپاتیت های ویرال:

TABLE 285-2 Clinical and Epidemiologic Features of Viral Hepatitis

Feature HAV HBV HCV HDV HEV Incubation (days) 15–45, mean 30 30–180, mean 60–90 15–160, mean 50 30–180, mean 60–90 14–60, mean 40 Onset Acute Insidious or acute Insidious Insidious or acute Acute Age preference Children, young adults Young adults (sexual and percutaneous), babies, toddlers Any age, but more common in adults Any age (similar to HBV) Young adults (20–40 years)   Fecal-oral +++ - - - +++   Percutaneous Unusual +++ +++ +++ -   Perinatal - +++ ±a + -   Sexual ± ++ ±a ++ -   Severity Mild Occasionally severe Moderate Occasionally severe Mild   Fulminant 0.1% 0.1–1% 0.1% 5–20%b 1–2%e 20%خانمهای باردار   Progression to chronicity None Occasional (1–10%) (90% of neonates) Common (50–70% chronic hepatitis; 80–90% chronic infection) Commond None   Carrier None 0.1–30%c 1.5–3.2% Variablef None   Cancer None + (neonatal infection) + ± None   Prognosis Excellent Worse with age, debility Moderate Acute, good Chronic, poor Good Prophylaxis IG Inactivated vaccine HBIG Recombinant vaccine None HBV vaccine (none for HBV carriers) Unknown Therapy None Interferon LamivudineAdefovir Pegylated interferon plus ribavirin Interferon ± None a Primarily with HIV co-infection and high-level viremia in index case; risk ~5%. b Up to 5% in acute HBV/HDV co-infection; up to 20% in HDV superinfection of chronic HBV infection. c Varies considerably throughout the world and in subpopulations within countries; see text. d In acute HBV/HDV co-infection, the frequency of chronicity is the same as that for HBV; in HDV superinfection, chronicity is invariable. e 10–20% in pregnant women. f Common in Mediterranean countries, rare in North America and western Europe.

The acute level of these enzymes, however, does not correlate well with the degree of liver cell damage. Peak levels vary from 400 to 4000 IU or more;

Bilirubin levels >340 µmol/L (20 mg/dL) extending and persisting late into the course of viral hepatitis are more likely to be associated with severe disease.

Hepatitis Aپروفیلاکسی پیش و پس از تماس در هپاتیت

Hepatitis A vaccines are approved for use in persons who are at least 2 years old and appear to provide adequate protection 4 weeks after a primary inoculation.

If it can be given within 4 weeks of an expected exposure, such as by travel to an endemic area, hepatitis A vaccine is the preferred approach to preexposure immunoprophylaxis

If travel is more imminent, IG (0.02 mL/kg) should be administered at a different injection site, along with the first dose of vaccine.

When administered before exposure or during the early incubation period, IG is effective in preventing clinically apparent hepatitis.

For postexposure prophylaxis of intimate contacts (household, sexual, institutional) of persons with hepatitis A, the administration of 0.02 mL/kg is recommended as early after exposure as possible; it may be effective even when administered as late as 2 weeks after exposure.

Prophylaxis is not necessary for casual contacts (office, factory, school, or hospital), for most elderly persons, who are very likely to be immune, or for those known to have anti-HAV in their serum.

For travelers to tropical countries, developing countries, and other areas outside standard tourist routes, IG prophylaxis had been recommended, before a vaccine became available!!!. When such travel lasted less than 3 months, 0.02 mL/kg was given; for longer travel or residence in these areas, a dose of 0.06 mL/kg every 4 to 6 months was recommended.

Hepatitis B

We now recognize that many cases of hepatitis B result from less obvious modes of nonpercutaneous or covert percutaneous transmission.

Perinatal transmission occurs primarily in infants born to HBsAg carrier mothers or mothers with acute hepatitis B during the third trimester of pregnancy or during the early postpartum period.

Perinatal transmission is uncommon in North America and western Europe but occurs with great frequency and is the most important mode of HBV perpetuation in the Far East and developing countries.

ویروس هپاتیت B پره کور-موتانت: هپاتیت مزمن شدید- سطوح پایین  HBV DNA مثبت -  HBe Ag منفی - AntiHBe Ab مثبت- نوسانات متناوب در فعالیت نکروز التهابی کبد- شایعترین نوع هپاتیت در مدیترانه و اروپا

Patients with such precore mutants that are unable to secrete HBeAg tend to have severe liver disease that progresses more rapidly to cirrhosis.

They have severe chronic HBV infection and detectable HBV DNA but with anti-HBe instead of HBeAg. These patients were found to be infected with an HBV mutant that contained an alteration in the precore region rendering the virus incapable of encoding HBeAg.

 Both “wild-type” HBV and precore-mutant HBV can coexist in the same patient, or mutant HBV may arise late during wild-type HBV infection.

Precore-mutant hepatitis B is now the most frequently encountered form of hepatitis B in Mediterranean countries and in Europe

Characteristic of such HBeAg-negative chronic hepatitis B are lower levels of HBV DNA and periodic fluctuations in hepatic necroinflammatory activity.

اسکیپ موتانت: در اثر جهش HBsAg خاصیت ایمنونیزاسیون اکتیو و پاسیو از بین می رود و افراد را علیرغم ایمن سازی به هپاتیت B مبتلا می سازد.

The second important category of HBV mutants consists of escape mutants, in which a single amino acid substitution, from glycine to arginine, occurs at position 145 of the immunodominant a determinant common to all subtypes of HBsAg. This change in HBsAg leads to a critical conformational change that results in a loss of neutralizing activity by anti-HBs. This specific HBV/a mutant has been observed in two situations, active and passive immunization

Although the precise mode of perinatal transmission is unknown, and although approximately 10% of infections may be acquired in utero, epidemiologic evidence suggests that most infections occur approximately at the time of delivery and are not related to breast feeding.

The likelihood of perinatal transmission of HBV correlates with the presence of HBeAg;

90% of HBeAg-positive mothers but

only 10 to 15% of anti-HBe-positive mothers

transmit HBV infection to their offspring.

In most cases, acute infection in the neonate is clinically asymptomatic, but the child is very likely to become an HBsAg carrier.

Pregnancy is not a contraindication to vaccination.

For unvaccinated persons sustaining an exposure to HBV, postexposure prophylaxis with a combination of HBIG (for rapid achievement of high-titer circulating anti-HBs) and hepatitis B vaccine (for achievement of long-lasting immunity as well as its apparent efficacy in attenuating clinical illness after exposure) is recommended.

For perinatal exposure of infants born to HBsAg-positive mothers, a single dose of HBIG, 0.5 mL, should be administered intramuscularly in the thigh immediately after birth, followed by a complete course of three injections of recombinant hepatitis B vaccine  to be started within the first 12 h of life.

For those experiencing a direct percutaneous inoculation or transmucosal exposure to HBsAg-positive blood or body fluids (e.g., accidental needle stick, other mucosal penetration, or ingestion), a single intramuscular dose of HBIG, 0.06 mL/kg, administered as soon after exposure as possible, is followed by a complete course of hepatitis B vaccine to begin within the first week.

For those exposed by sexual contact to a patient with acute hepatitis B, a single intramuscular dose of HBIG, 0.06 mL/kg, should be given within 14 days of exposure, to be followed by a complete course of hepatitis B vaccine.

When both HBIG and hepatitis B vaccine are recommended, they may be given at the same time but at separate sites.

Approximately 80 to 90% of immunocompetent vaccinees retain protective levels of anti-HBs for at least 5 years, and 60 to 80% for 10 years.

 Currently, booster immunizations are not recommended routinely, except in immunosuppressed persons who have lost detectable anti-HBs or immunocompetent persons who sustain percutaneous HBsAg-positive inoculations after losing detectable antibody.

Specifically, for hemodialysis patients, annual anti-HBs testing is recommended after vaccination; booster doses are recommended when anti-HBs levels fall below 10 mIU/mL.

TABLE 285-3 Commonly Encountered Serologic Patterns of Hepatitis B Infection

HBsAg Anti-HBs Anti-HBc HBeAg Anti-HBe Interpretation + - IgM + - Acute hepatitis B, high infectivity + - IgG + - Chronic hepatitis B, high infectivity (Wild type) Load:105 + - IgG - + 1.  Late acute or chronic hepatitis B, low infectivity 2.  HBeAg-negative (“precore-mutant”) hepatitis B (chronic or, rarely, acute)بار ویروسی زیاد + + + +/- +/- 1.  HBsAg of one subtype and heterotypic anti-HBs (common) 2.  Process of seroconversion from HBsAg to anti-HBs (rare) - - IgM +/- +/- 1.  Acute hepatitis B 2.  Anti-HBc “window” - - IgG - +/- 1.  Low-level hepatitis B carrier 2.  Hepatitis B in remote past - + IgG - +/- Recovery from hepatitis B - + - - - 1.  Immunization with HBsAg (after vaccination) 2.  Hepatitis B in the remote past (?) 3.  False-positive

ymphadenopathy.