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ACUTE VIRAL GASTROENTEROLOGY OUTLINE I. Introduction II. Hepatitis Viruses III. Signs & symptoms A. Incubation Period B. Prodromal Symptoms C. Clinical Jaundice D. Recovery Phase IV. Laboratory Findings A. First Subtopic B. Second Subtopic C. Third Subtopic D. Fourth Subtopic IV. Serologic Markers & Scheme V. Treatment VI. Complications I. INTRODUCTION Acute viral hepatitis- a systemic infection affecting the liver predominantly. Almost all cases of acute viral hepatitis are caused by one of five viral agents o HAV, HBV, HCV, HBV-associated delta agent or HDV, & HEV. All are RNA viruses o except for hep B: DNA virus but replicates like a retrovirus. II. HEPATITIS VIRUSES Please see appendix I for the features of the hepatitis viruses. Please see appendix II for the clinical & epidemiologic features of viral hepatitis. Prophylaxis & t herapeutics included on the table as well. III. SIGNS & SYMPTOMS A. Incubation Period Hepatitis A: 15–45 days, mean, 4 weeks Hepatitis B & D: 30–180 days, mean, 8–12 weeks Hepatitis C 15–160 days, mean, 7 weeks Hepatitis E 14–60 days, mean, 5–6 weeks B. Prodromal Symptoms 1-2 weeks before jaundice o Constitutional symptoms: anorexia, nausea and vomiting (associated with alterations in olfaction and taste), fatigue, malaise, arthralgias, myalgias, headache, photophobia, pharyngitis, cough, and coryza o low-grade fever between 38°-39°C (100°-102°F) is more often present in hepatitis A & E than in hepatitis B or C, except when hepatitis B is heralded by a serum sickness–like syndrome o rarely, fever of 39.5°–40°C (103°– 104°F) 1–5 days before the onset of clinical jaundice o Dark urine and clay-colored stools may be noticed B. Clinical Jaundice constitutional prodromal symptoms usually diminish in some, mild weight loss (2.5–5 kg) is common and may continue during the entire icteric phase liver becomes enlarged and tender and may be associated with RUQ pain and discomfort. present with a cholestatic picture, suggesting extrahepatic biliary obstruction (infrequent) splenomegaly and cervical adenopathy (in 10–20%) spider angiomas appear during the icteric phase and disappear during convalescence (rare) C. Recovery Phase constitutional symptoms disappear usually some liver enlargement and abnormalities in liver biochemical tests are still evident. duration of the posticteric phase is variable (2-12 weeks) o usually more prolonged in acute hepatitis B & C Complete clinical and biochemical recovery: o 1–2 months after hepatitis A and E o 3–4 months after the onset of jaundice in ¾ of uncomplicated, self-limited cases of hepatitis B (95-99%) and C (~15%). o biochemical recovery may be delayed III. LABORATORY FINDINGS AST & ALT o during prodromal phase of acute viral hepatitis & precede the rise in bilirubin Page 1 of 4 | Laxamana, Trisha D.

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Acute Viral Hepatitis

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OUTLINEI. Introduction II. Hepatitis VirusesIII. Signs & symptomsA. Incubation PeriodB. Prodromal SymptomsC. Clinical JaundiceD. Recovery Phase

IV. Laboratory FindingsA. First SubtopicB. Second SubtopicC. Third SubtopicD. Fourth SubtopicIV. Serologic Markers & SchemeV. TreatmentVI. Complications

I. INTRODUCTION Acute viral hepatitis- a systemic infection affecting the liver predominantly. Almost all cases of acute viral hepatitis are caused by one of five viral agents HAV, HBV, HCV, HBV-associated delta agent or HDV, & HEV. All are RNA viruses except for hep B: DNA virus but replicates like a retrovirus.

II. HEPATITIS VIRUSES Please see appendix I for the features of the hepatitis viruses. Please see appendix II for the clinical & epidemiologic features of viral hepatitis. Prophylaxis & t herapeutics included on the table as well.

III. SIGNS & SYMPTOMSA. Incubation Period Hepatitis A: 1545 days, mean, 4 weeks Hepatitis B & D: 30180 days, mean, 812 weeks Hepatitis C 15160 days, mean, 7 weeks Hepatitis E 1460 days, mean, 56 weeks

B. Prodromal Symptoms 1-2 weeks before jaundice Constitutional symptoms: anorexia, nausea and vomiting (associated with alterations in olfaction and taste), fatigue, malaise, arthralgias, myalgias, headache, photophobia, pharyngitis, cough, and coryza low-grade fever between 38-39C (100-102F) is more often present in hepatitis A & E than in hepatitis B or C, except when hepatitis B is heralded by a serum sicknesslike syndrome rarely, fever of 39.540C (103104F) 15 days before the onset of clinical jaundice Dark urine and clay-colored stools may be noticed

B. Clinical Jaundice constitutional prodromal symptoms usually diminish in some, mild weight loss (2.55 kg) is common and may continue during the entire icteric phase liver becomes enlarged and tender and may be associated with RUQ pain and discomfort. present with a cholestatic picture, suggesting extrahepatic biliary obstruction (infrequent) splenomegaly and cervical adenopathy (in 1020%) spider angiomas appear during the icteric phase and disappear during convalescence (rare)

C. Recovery Phase constitutional symptoms disappear usually some liver enlargement and abnormalities in liver biochemical tests are still evident. duration of the posticteric phase is variable (2-12 weeks) usually more prolonged in acute hepatitis B & C Complete clinical and biochemical recovery: 12 months after hepatitis A and E 34 months after the onset of jaundice in of uncomplicated, self-limited cases of hepatitis B (95-99%) and C (~15%). biochemical recovery may be delayed III. LABORATORY FINDINGS AST & ALT during prodromal phase of acute viral hepatitis & precede the rise in bilirubin however, rise does not correlate well with the degree of liver cell damage. Peak levels: 4004000 IU or more usually reached at the time the patient is clinically icteric diminish progressively during recovery diagnosis of anicteric hepatitis- based on clinical features and on aminotransferase elevations Bilirubin Jaundice is usually visible in the sclera or skin when s >43 mol/L (2.5 mg/dL) continue to rise despite falling serum aminotransferase levels. usually the total bilirubin is equally divided between the conjugated and unconjugated fractions

Transiet neutropenia & lymphopenia followed by relative lymphocytosis. Prolonged PT may reflect a severe hepatic synthetic defect, signify extensive hepatocellular necrosis, and indicate a worse prognosis Hypoglycemia In severe cases d/t nausea &vomiting, inadequate carbohydrate intake, & poor hepatic glycogen reserves may contribute to hypoglycemia noted occasionally Alkaline phosphatas- normal or mildly elevated In some patients: mild and transient steatorrhea slight microscopic hematuria Minimal proteinuria

IV. SEROLOGIC MARKER & SCHEME

A. Hepatitis (General)

B. Hepatitis A

C. Hepatitis B

D. Hepatitis C

V. TREATMENT Only supportive measures For acute HCV- PEG Interferon plus ribavirin for 24 weeksVI. COMPLICATIONS Relapsing Hepatitis A Cholestatic Hepatitis A Fulminant Hepatitis most feared; rare seen primarily in hepatitis B, D, and E, but rare fulminant cases of hepatitis A Chronic hepatitis important late complication of acute hepatitis B in small proportion of patients with acute disease but more common in those who present with chronic infection withouthaving experienced an acute illness, as occurs typically after neonatal infection or after infection in an immunosuppressed host Rare complications: pancreatitis, myocarditis, atypical pneumonia, aplastic anemia, transverse myelitis, and peripheral neuropathy.

ACUTE VIRAL HEPATITISGASTROENTEROLOGY

Topic

| Laxamana, Trisha D.

III. APPENDIX