Hepatitis

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Hepatitis in children

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PowerPoint Presentation:

Hepatitis G.Reza Jeloudar MD بسم الله الرحمن الرحیم

The Liver:

The Liver Is located in the upper right quadrant of the abdomen Cleans the blood Regulates hormones Helps with blood clotting Produces bile Produces important proteins Maintains blood sugar levels And much, much, more The liver is essential for life !

What Is Hepatitis?:

What Is Hepatitis? Hepatitis means inflammation of the liver Hepat (liver) + itis (inflammation)= Hepatitis Viral hepatitis means there is a specific virus that is causing your liver to inflame (swell or become larger than normal)

Hepatomegaly:

Hepatomegaly Concepts of normal liver size have been based on age-related clinical indices, such as ( 1 ) the degree of extension of the liver edge below the costal margin ; ( 2 ) the span of dullness to percussion ; or ( 3 ) the length of the vertical axis of the liver, as estimated from imaging techniques.

PowerPoint Presentation:

In children, the normal liver edge can be felt up to 2 cm below the right costal margin. In a newborn infant, extension of the liver edge more than 3.5 cm below the costal margin in the right midclavicular line suggests hepatic enlargement

Evaluation of Patients with Possible Liver Dysfunction :

Evaluation of Patients with Possible Liver Dysfunction History : Drug, injection, FHx of Dx P/E : scleral, mucosal, cutaneous icterus, hepatosplenomegaly , ascites, edema,clubbing,petechiae , ecchymosis

Biochemical Tests:

Biochemical Tests serum transaminase (ALT,AST) bilirubin (total and fractionated) alkaline phosphatase (AP) levels prothrombin time (PT) or(INR) albumin level Imaging Liver Biopsy

Causes and Differential Diagnosis of Hepatitis in Children :

Causes and Differential Diagnosis of Hepatitis in Children

ISSUES COMMON TO ALL FORMS OF VIRAL HEPATITIS:

ISSUES COMMON TO ALL FORMS OF VIRAL HEPATITIS Often what brings the patient with hepatitis to medical attention is clinical icterus The liver is usually enlarged and tender to palpation and percussion Splenomegaly and LAP can be present

Common Biochemical Profiles in the Acute Infectious Phase:

Common Biochemical Profiles in the Acute Infectious Phase cytopathic injury: rise in serum level of ALT , AST Cholestasis : defined by elevated serum conjugated bilirubin levels Synthetic function: protein synthesis (prolonged PT, high INR, low serum alb levels), metabolic disturbances (hypoglycemia, lactic acidosis, hyperammonemia), poor clearance of medications , and altered sensorium with increased deep tendon reflexes ( hepatic encephalopathy )

HEPATITIS A:

HEPATITIS A the most prevalent of the 5 V. HAV is an RNA virus HAV is highly contagious Transmission is almost always by person-to-person contact through the fecal-oral route

Clinical Manifestations:

Clinical Manifestations Mean incubation period is 3 wk acute hepatitis only Often this is an anicteric illness Like viral gastroenteritis acute febrile illness ,anorexia, nausea, malaise, vomiting, and jaundice duration of illness is 7-14 days

Diagnosis:

Diagnosis Acute infection:anti-HAV (IgM) PCR HAV (IgG) Rises in serum levels of ALT, AST, bilirubin, ALP, 5'-nucleotidase, and GGT

Complications:

Complications most patients achieve full recovery ALF from HAV infection is a rare but not infrequent prolonged cholestatic syndrome (Pruritus and fat malabsorption)

Treatment:

Treatment Supportive treatment (intravenous hydration and antipruritic and fat-soluble vitamins) Serial monitoring for signs of ALF transplantation center (ALF)

Prevention:

Prevention contagious for 2 wk before and 7 days after the onset of jaundice Careful handwashing IG (0.02 ml/kg) effective protection for up to 3 mo ( before travel, <1 yr, allergic to a vaccine, immunocompromised) VACCINE: 2-dose the 2nd dose given 6-12 mo after the 1st

HEPATITIS B:

HEPATITIS B DNA virus 4 genes have been identified: S(surface), C (core), X, P(polymer) Worldwide infection highest incidence 20-39 yr of age high concentrations: blood,serum, exudates moderate concentrations : saliva, vaginal fluid, semen

PowerPoint Presentation:

In children, the most important risk factor for acquisition of HBV remains perinatal exposure to an HBsAg-positive mother the incubation period 45 to 160 days, mean 120 days

Clinical Manifestations:

Clinical Manifestations Many acute cases in children are asymptomatic similar to that of HAV and HCV elevation of serum ALT levels fatigue, anorexia, and malaise, 6-7 wk after exposure serum sickness-like prodrome (arthralgia or skin lesions, including urticarial, purpuric , macular,or maculopapular rashes) Jaundice(8 wk after exposure)

Diagnosis:

Diagnosis Routine screening for HBV :3 serologic markers (HBsAg, antiHBc , anti-HBs)

Complications:

Complications ALF (occurs more commonly with HBV): coagulopathy, encephalopathy, and cerebral edema chronic hepatitis Cirrhosis hepatocellular carcinoma Membranous glomerulonephritis

Treatment:

Treatment Supportive Interferon-α-2b (IFN-α2b) Lamivudine Prevention Vaccine HBIG

HEPATITIS C:

HEPATITIS C RNA virus Transmission :Illegal drug exposure to blood or blood products Sexual perinatal (the most prevalent mode in children) incubation period : 7-9 wk (range, 2-24 wk )

Clinical Manifestations:

Clinical Manifestations Acute HCV:mild and insidious ALF: rarely occurs Chronic HCV :silent until a complication develops Serum aminotransferase levels fluctuate

Diagnosis:

Diagnosis anti-HCV Ab viral RNA PCR

Complications:

Complications chronic hepatitis Peginterferon + ribavirin No vaccine Treatment Prevention

HEPATITIS D:

HEPATITIS D cannot produce infection without HBV(co-infection, super-infection) symptoms are similar to but usually more severe than those of the other hepatotropic viruse Diagnosis: Anti-HDV Ab IgM Treatment : supportive

HEPATITIS E:

HEPATITIS E has not been isolated non-A, non-B hepatitis Transmission is fecal-oral Clinical Manifestations: similar to that of HAV but is often more severe major pathogen in pregnant women Diagnosis: Anti-HEV Ab

Wilson Disease (hepatolenticular degeneration):

Wilson Disease (hepatolenticular degeneration) Autosomal recessive Degenerative changes in the brain, liver disease, and Kayser-Fleischer rings in the cornea Progressive and potentially fatal if untreated

PATHOGENESIS:

PATHOGENESIS Gene P-type ATPase decreased biliary copper excretion and diffuse accumulation of copper in the cytosol of hepatocytes, brain and kidneys

CLINICAL MANIFESTATIONS:

CLINICAL MANIFESTATIONS Asymptomatic hepatomegaly Subacute or chronic hepatitis Cirrhosis younger patient: hepatic involvement Neurologic: intention tremor, dysarthria, rigid dystonia, parkinsonism,choreiform movements, behavioral changes

PowerPoint Presentation:

Kayser-Fleischer rings Psychiatric manifestations include depression, personality changes, anxiety, psychosis Coombs-negative hemolytic anemia

DIAGNOSIS:

DIAGNOSIS children and teenagers with: unexplained acute or chronic liver disease neurologic symptoms of unknown cause acute hemolysis psychiatric illnesses Fanconi syndrome unexplained bone(osteoporosis, fractures) or muscle disease (myopathy, arthralgia).

TREATMENT: restrict dietary copper intake Foods such as liver, shellfish, nuts, and chocolate should be avoided copper-chelating agents:D-penicillamine Zinc :

TREATMENT: restrict dietary copper intake Foods such as liver, shellfish, nuts, and chocolate should be avoided copper-chelating agents :D-penicillamine Zinc decreased ceruloplasmin levels serum copper: elevated in early urinary copper excretion increased Liver biopsy

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